Posts Tagged ‘cognitive neuroscience’

System 2 Processing and a Healthy Democracy

May 1, 2020

The immediately preceding post stressed the importance of System 2 Processing to prevent Alzheimer’s and dementia, and to live a more fulfilling life. As the title of this post implies, System 2 Processing is necessary for a healthy democracy.

To briefly review the previous post, this blog has many citations of Kahneman’s Two System Theory of Cognitive Processing. System 1 is our most common mode of processing. It is fast and efficient. Unfortunately, this speed is paid for at a cost. The failure to think critically can be disastrous in more important decisions. Cognitive neuroscience, which conducts brain imaging studies, has a term for mental activity which is the typical norm, called, accordingly, default mode processing. This mode can be identified in brain images. The default network of interacting brain regions is known to have activity highly correlated with each other and distinct from other networks in the brain. These regions are negatively correlated with attention networks in the brain. Normal conversation and well performed tasks are System 1 activities. Thinking and learning are System 2 processes, and they involve cognitive effort. Most of the time spent on social media involves System 1 processing primarily.

A successful democracy also requires System 2 processing. Trump works only through System 1 processing. System 1 processing is emotional. He targets hate groups, illegal immigrants, and others and proposes simplistic solutions. He is also a hypocrite. The simplest and best solution to illegal immigration is to severely fine and even imprison people who hire illegal immigrants. Foremost among these people is Donald Trump. He likes to hire illegals because they are easy to exploit. So it is clear that Trump supporters are not doing any System 2 processing

Many laborers are strong Trump supporters. But Trump’s common mode of developing is to abandon the project and leave the workers unpaid. He is no friend of labor; he is an exploiter of labor. So any laborer who supports Trump is dong little, if any, System 2 processing.

Previous posts, see the House of Trump, the House of Putin show a long time relationship with Russia. His credit was so bad in the United States, that no lender would lend him money. Yet Trump kept building expensive properties. His son said he could do this because Russia had no problem lending him money. Previous posts have argued that Trump needs to explain where his funds came from. He refuses to do so, and the reason he hides his taxes, is that they would reveal how he is compromised with Russia.

Now we come to the Coronavirus. Although a majority of respondents think Trump is doing a poor job only several percentage points indicate that many do support Trump’s job. First of all, Trump has done his best to defund or underfund all scientific enterprises. The Obama administration also left a plan for dealing with this epidemic, but Trump had the plan destroyed. In the first days he denied that there was a pandemic and accused this pandemic of being false news generated by the Democrats to keep him from being elected. When he did admit that there was an epidemic, he said that there was a test, a beautiful test for the disease that was readily available. It was not, and as of the writing of this post, it is still not available. The lack of this test is a very large, if not the largest, shortcoming damaging the fight against this pandemic.

Eventually, Trump said he was taking charge and was the general fighting this disease. But he has been an ineffective general, and it can be argued that he has done more damage than good. Rather than lead the fight as a general should do, he says that this is for the states to handle. Now the declaration of a national emergency is done to put the federal government, the President, in charge of the battle. The National War Powers Act gives the President the power do this, but although he has activated the National War Powers Act he has not used it. Consequently states are competing against each other and FEMA trying to get necessary equipment. This not only slows delivery, but greatly increases costs.

Yet a large percentage of people believe he is doing a good job. This is based on the lies he is telling them. No System 2 processing is being done that would correctly indicate that Trump is lying.

This absence of System 2 processing where it is needed could lead to Trump’s reelection. And that would likely be the end of American democracy.

© Douglas Griffith and healthymemory.wordpress.com, 2020. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

For Alzheimer’s, An Elusive Cure

April 30, 2020

The title of this post is identical to the title of an article by Christie Aschwanden in The Health & Science Section of The Washington Post. The article states, “For a decade over 200 leads have failed. Today, experts say the disease is more complex than first believed.” The defining features for a diagnose of Alzheimer’s are neurofibrillary tangles and amyloid plaque. The cure they are seeking are drugs that prevent or remove these substances from the brain.

What is not mentioned in this article, and is rarely mentioned in any article, is that autopsies have revealed many people with brains full of these defining features, but who never exhibited any of the behavioral or cognitive symptoms. Now it is these behavioral and cognitive symptoms that are what is important, not the defining features of plaques and tangles. These people, who clearly would be diagnosed with Alzheimer’s, never suffered any of the behavioral or cognitive symptoms.

The reason provided for these people was that they had built up cognitive reserves that defended them from adverse effects of the defining features of Alzheimer’s. There are previous healthy memory blog posts on this important finding. Alzheimer’s and Amyloid Plaques was posted on July 6, 2011. That article stated that amyloid plaque was a necessary but not a sufficient factor for Alzheimer’s. On May 8, 2011 a second healthy memory blog post titled Glial Cells and Alzheimer’s Disease addressed this issue.

But the single, most important post was on August 28, 2011, The Myth of Alzheimer’s. The Myth of Alzheimer’s is a book by Peter J. Whitehouse, M.D. & Ph.D., and Daniel George, M.Sci. Dr. Whithouse had spent many years looking for a medicinal cure or preventative for Alzheimer’s. He was highly compensated for his work, and could have continued working on this topic. But he became convinced that this research would never yield fruit. He continued researching Alzheimer’s, but stopped his research looking for a medicinal prevention or cure. It is nine years later and researchers are continuing research, but have realized that the disease is more complex than first believed, so they are pursuing multiple medicines. It is clear why this research is continuing as financial rewards would be enormous, especially if multiple medications are needed.

Although cures are not in the offing, it appears that the preventive measures are clear. The preventive measures involve developing a cognitive reserve. People who have developed a cognitive reserve have been mentally active throughout their lives. This blog has many citations of Kahneman’s Two System Theory of Cognitive Processing. System 1 is our most common mode of processing. It is fast and efficient. Unfortunately, this speed is paid for at a cost. The failure to think critically can be disastrous in more important decisions. Cognitive neuroscience, which conducts brain imaging studies, has a term for mental activity which is the typical norm, called accordingly default mode processing. This mode can be identified in brain images. The default network of interacting brain regions is known to have activity highly correlated with each other and distinct from other networks in the brain. These regions are negatively correlated with attention networks in the brain. Normal conversation and well performed tasks are System 1 activities. Thinking and learning are System 2 processes and they involve cognitive effort. Most of the time spent on social media involves System 1 processing primarily.

The healthy memory blog recommends growth mindsets throughout one’s lifetime. Continue to think critically, and learn. In addition to increasing the odds against Alzheimer’s or dementia, it also provides for a richer, fuller life with a healthy memory. A healthy memory among the citizenry is important to a democracy.

The Post article does mention that some of the most promising approaches to addressing Alzheimer’s are nonpharmaceutical. The NIA is sponsoring 86 studies of non drug interventions that may help, including exercising, diet, cognitive training and sleep.

A study conducted in Finland and published in 2015, found that a program of physical activity, cognitive stimulation, a Mediterranean diet including fish offered some protection against cognitive decline. Participants were at a risk for dementia, but none had it. After two years, the risk of exhibiting cognitive decline was his 30% higher in the control group than in the one assigned to the lifestyle interventions. But what is needed is a lifestyle change, not just an intervention, although an intervention apparently does achieve some benefit.

It should be clear that System 2 cognitive processes are essential, but a healthy lifestyle is also essential. HM has a personal friend who, on the basis of his cognitive activity, one would think would be the last person to suffer Alzheimer’s. However, he had trained himself to sleep only 4 hours a night, so he could enjoy more waking time. But it appears that this was a poor tradeoff.

© Douglas Griffith and healthymemory.wordpress.com, 2020. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Healing Your Identity

April 15, 2020

This post is the thirteenth on an essential book by Jeffrey Rediger, M.D. titled Cured: The Life-Changing Science of Spontaneous Healing. The title of this post is the same as the title of a chapter in that book. Dr. Rediger is a psychiatrist, and this is a chapter where it is quite clear that he is a psychiatrist.

Drs.Vincent Felitti and Richard Anda identified ten types of childhood stress and trauma that they called adverse childhood experiences or ACEs. Here is the list

Physical abuse
Sexual abuse
Emotional abuse
Physical neglect
Emotional neglect
Exposure to domestic violence
Household domestics abuse
Household mental illness
Parental separation or divorce
Incarcerated household member

These adverse childhood experiences can result in serious emotional damage that can be carried throughout one’s life. Dr. Rediger brings in the concept of a default mode network (DMN). As the name implies, the default mode is the mode to which the brain defaults when it is not actively thinking. Dr. Redger says that for him, moving beyond childhood trauma and making sure his body wasn’t locked into a cycle of chronic fight or flight also meant getting out of his default mode network.

He writes, “New experiences are one way to do this; any time you get out of your daily routine and experience something new, your brain exits the DMN, and you get out of your default mode of operating. It’s an enormous opportunity both for changing your thought patterns and changing your health. When you get out of the the DMN, you have the chance to create and reinforce new neural pathways that can override existing ones.

The concept of the DMN should not be new to regular readers of the healthy memory blog (e.g, “Default Network, System 1 Processing, and Alzheimer’s Disease.) Enter “Default Network” into the search block at healthymemory.wordpress.com
to find that post.

That post identified similarities between the default mode network and Kahneman’s System 1 Processing. Kahneman’s System 1 processing is important in that HM thinks that too heavy a use of System 1 processing at the expense of System 2 processing, which is active thinking, increases the risk for AD.

The simplest distinction between the two terms is that Kahneman is a cognitive psychologist and his two process view of cognitive processes comes from cognitive psychology. The default mode network comes from cognitive neuroscience. Default mode activity is identified via brain imaging. Although they might not be identical, that distinction awaits further research, it is clear that there is considerable overlap between the two.

In addition to brain atrophy, AD patients have abnormal high levels of proteins in different brain regions. In the medial temporal lobe, the accumulation of tau protein leads to neurofibrillary tangles. In cortical regions, such as the parietal cortex in early AD, the accumulation of amyloid-B protein leads to amyloid plaques. The neurofibrillary tangles in the medial temporal lobe and amyloid plaques in cortical regions can be assumed to disrupt neural processing in these regions.

Dr. Slotnick writes, “There is an influential hypothesis that there is a causal relationship between default network activity that leads to deposition of amyloid that results in atrophy and disrupted metabolic activity, which impairs long-term memory in AD patients. The regions in the default network are active when participants are not engaged in a task and include the dorsolateral prefrontal cortex, the medial prefrontal cortex, the inferior prefrontal cortex and the medial parietal cortex. In AD patients, amyloid deposition occurs in the same regions, which suggests the default network activity may lead to amyloid deposition. Dr. Slotnick suggests that perhaps higher levels of amyloid deposition, which occurs in late AD patients, is necessary to produce atrophy in the frontal cortex.

Dr. Slotnick continues, “If high amyloid deposition is a causal factor in developing AD, older adults with low levels of amyloid should be at decreased risk for developing this disease. There is some evidence that cognitive engagement throughout life may reduce the amyloid level in the brains of healthy older adults as a function of cognitive engagement, and this was compared to the cortical amyloid levels . Participants rated the frequency which they engaged in cognitively demanding tasks such as reading, writing, going to the library, or playing games at five different ages (6, 12, 18, 40, and their current age). Healthy older adults with greater cognitive engagement throughout their lifetime, as measured by the average cognitive activity at the five ages, had lower levels of amyloid in default network regions. Moreover, the healthy older adults in the lowest one-third of lifetime engagement had amyloid levels that were equivalent to AD patients, and the healthy older adults in the highest one-third of lifetime cognitive engagement had amyloid levels that were equivalent to young adults.

Dr. Rediger is arguing that another reason for exiting DFM and reviewing and forgetting ACEs, is that it will facilitate the healing of your identity, which, in addition to the other factors he identifies in his book, might facilitate a spontaneous remission.

Alzheimer’s Disease (AD)

September 24, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

As AD progresses from earlier to later stages, atrophy starts in the medial temporal lobe, extends to the parietal lobe, and finally includes the frontal lobe. The long-term memory impairment in early AD patients can be attributed to the disrupted processing in the hippocampus and parietal cortex, to regions that have been associated with this cognitive process. As the disease progresses, other cognitive processes are disrupted such as attention and language, which both depend on the dorsolateral prefrontal cortex.

In early AD patients, as atrophy begins in the parietal cortex and the frontal cortex, there have also been reports of increases in fMRI activity within cortical regions. It is unknown whether these increases in cortical fMRI activity reflect a compensatory mechanism, which is often assumed to be the case, or reflect non-compensatory hyperactivity due to neural disruption.

In addition to brain atrophy, AD patients have abnormal high levels of proteins in different brain regions. In the medial temporal lobe, the accumulation of tau protein leads to neurofibrillary tangles. In cortical regions, such as the parietal cortex in early AD, the accumulation of amyloid-B protein leads to amyloid plaques. The neurofibrillary tangles in the medial temporal lobe and amyloid plaques in cortical regions can be assumed to disrupt neural processing in these regions.

Dr. Slotnick writes, “There is an influential hypothesis that there is a causal relationship between default network activity that leads to deposition of amyloid that results in atrophy and disrupted metabolic activity, which impairs long-term memory in AD patients. The regions in the default network are active when participants are not engaged in a task and include the dorsolateral prefrontal cortex, the medial prefrontal cortex, the inferior prefrontal cortex and the medial parietal cortex. In AD patients, amyloid deposition occurs in the same regions, which suggest the default network activity may lead to amyloid deposition. Dr. Slotnick suggests that perhaps higher level of amyloid deposition, which occurs in late AD patients, is necessary to produce atrophy in the frontal cortex.

Healthy memory readers should recognize the similarity between the default network and Kahneman’s System 1 processing. System 1 processing is the default network that needs to be disrupted to engage in System 2 processing, better known as thinking.

Dr. Slotnick continues, “If high amyloid deposition is a causal factor in developing AD, older adults with low levels of amyloid should be at decreased risk for developing this disease. There is some evidence that cognitive engagement and exercise throughout life may reduce the amyloid level in the brains of healthy older adults as a function of cognitive engagement (System 2 processing), and this was compared to the cortical amyloid levels . Participants rated the frequency which they engaged in cognitively demanding tasks such as reading, writing, going to the library, or playing games at five different ages (6, 12, 18, 40, and their current age). Healthy older adults with greater cognitive engagement throughout their lifetime, as measured by the average cognitive activity at the five ages, had lower levels of amyloid in default network regions. Moreover, the healthy older adults in the lowest one-third of lifetime engagement had amyloid levels that were equivalent to AD patients, and the healthy older adults in the highest one-third of lifetime cognitive engagement had amyloid levels that were equivalent to young adults.

It should also be noted that many have died who upon autopsy had levels of amyloid plaque and neurofibrillary tangles definitive of AD, but who never exhibited any of the behavioral or cognitive symptoms characteristics of the disease. The explanation typically offered for these individuals is that they had built a cognitive reserve as a result of the mental activities they had engaged in during their lifetimes.

There is a wide variety of products sold to prevent AD, such as computer games and pills that increase short-term memory. But it should be clear from the posts on cognitive science that the entire brain is involved. That is why the healthy memory blog strongly recommends growth mindsets with continual learning throughout the lifespan. These make heavy use of System 2 processing. Of course, a healthy lifestyle that includes physical exercise must also be part of the mix.

Transient Global Amnesia (TGA)

September 23, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

The criteria used to diagnose follow:
There is clear anterograde amnesia.
The attack must last no longer than 24 hours.
The individual must not have clouding of consciousness (drowsiness) and they must know their personal identity.
The attack must be witnessed by another person.
There should be no other neurological symptoms during or after the attack (problems speaking or partial paralysis).
There should be no recent history of head injury or epilepsy.

TGA patients often have retrograde amnesia for hours before the attack and have anterograde amnesia for 1 to 10 hours. They usually repeat the same questions, such as “where am I?” and “why am I here?” because they forget that they had already asked a question and received an answer. The most common events that precipitate an attack are emotional stress, physical effort, contact with hot or cold water, or sexual intercourse. TGA patients are usually middle-aged or elderly adults. Accompanying symptoms can include headache, nausea, and dizziness. After diagnosis, the course of treatment is to wait for the amnesia to resolve on its own.

Research provides compelling evidence that TGA is caused by a temporary lesion in the CA1 region of the hippocampus. This is consistent with the important role of the hippocampus in long term memory. The mechanism underlying hippocampal lesions in TGA patients remains unknown. One hypothesis is that TGA patients have blood flow problems due to vascular blockage, but TGA patients do not have greater vascular risk
factors, such as high blood pressure, high cholesterol, than healthy control participants.

Dr. Slotnick writes, “The only identified risk factor is a history of migraine headaches. As emotional or physical stress almost always triggers TGA attacks and stress can produce changes in blood flow, it may be that hippocampal CA2 lesions are due to stress-induced decreases in blood flow to this sub-region. The hippocampal CA1 sub-region may be particularly susceptible to reductions in blood flow because it is supplied by one large artery, while the other hippocampal sub-regions are supplied by one large artery and many small arteries. The temporary focal lesions in the hipocampas CA1 sub-region of TGA patients provide a unique opportunity for future collaborations between cognitive neuroscientists and neurologists to investigate the specific role of this region in long-term memory.

Mild Traumatic Brain Imagery (mTBI)

September 22, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Patients with mTBI do not have any brain abnormalities, as measured using structural neuroimaging methods such as anatomic MRI. The diagnosis of mTBI includes loss of consciousness for less than 30 minutes and post-traumatic amnesia for less than 24 hours. Patients with mTBI can have attention and memory deficits, but these typically resolve within a few weeks.

The performance between mTBI patients and control participants did not differ on the memory task they were performing, but the mTBI patients had a greater extent and magnitude of fMRI activity in the dorsolateral prefrontal cortex and the parietal cortex than control participants.

Fifteen mTBI patients with concussions due to sports-related injuries were tested 2 days, 2 weeks, and 2 months after the injury. Only one of the 15 patients still had symptoms 2 months after the injury. Consistent with the previous research, there were no differences in the performance of the memory task between the patients and the control participants, but there was greater fMRI activity in the mTBI patients than the control participants within the dorsolateral prefrontal cortex at all three time points and within the parietal cortex at the first two time points. This greater fMRI activity 2 months after injury is concerning because they indicate there are differences in brain processing even after behavioral symptoms have been resolved. So there can be persistent brain disruptions even though there are no behavioral symptoms or brain abnormalities observable with anatomic neuroimaging methods.

Dr. Slotnick writes, “As mTBI patients may be more sensitive to repeated head trauma, it is arguable that they should not be allowed to continue participating in impact sports until their fMRI activity returns to normal.

There is also evidence that the magnitude of fMRI activity decreases in mTBI imagery with more severe or repeated head injuries. One working memory fMRI study had mTBI patients with more severe sports-related head injuries. These not-so-mild mTBI patients were tested 1 to 14 months after the most recent head injury. The large majority of participants had multiple previous concussions, and 15 of the 16 participants had persistent symptoms. As before, behavioral measures did not differ on the memory tasks between the mTBI patients and the control subjects. There was greater activity in the dorsolateral prefrontal cortex for the control participants than in mTBI patients, in direct opposition to the previous findings for less severe mTBI patients. Additionally, participants with greater post-concussive symptoms had a smaller magnitude and extent of firm activity within the dorsolateral prefrontal cortex during visual working memory blocks. The same pattern of fMRI results was obtained in a subsequent study that employed the identical visual working memory task and a similar group of not-so-mild mTBI participants. It is important to realized that repeated mTBI and sub-concussive head injuries ( due to boxing or football, for example) can lead to chronic traumatic encephalopathy (CTE).

There are eleven previous posts addressing chronic traumatic encephalopathy.

Amnestic Mild Cognitive Impairment

September 21, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Amnestic mild cognitive impairment (aMCI) occurs in a small but significant percentage of adults who are older than 60 years of age, with incidence increasing as a function of age. Approximately 50% of these cases will become Alzheimer’s sufferers. Individuals with aMCI have a selective impairment in long-term memory as compared to healthy age-matched control participants, and are unimpaired in other cognitive domains. There is an increasing body of evidence indicating that the long-term memory impairment in aMCI patients is due to atrophy of medial temporal lobe sub regions that is increased by a paradoxical increase in fMRI activity within the medial temporal lobe.

Structural MRI was used to compare the size of the hippocampus and the entorhinal cortex in aMCI patients and control participants. aMCI patients had a smaller hippocampal value and a smaller entorhinal cortex volume in both hemispheres as compared to age-matched control participants, indicating atrophy of these regions. In addition, the white matter pathway between the entorhinal cortex and the hippocampus had a smaller volume in aMCI patients than control participants, and this was the only white matter region in the entire brain that differed in volume. These results indicate that the long-term memory impairments in aMCI patients are due to isolated atrophy in the entorhinal cortex and the hippocampus.

A relatively higher magnitude of fMRI activity within the CA3/DG sub-region during a pattern separation task reflects a non-compensatory change in processing related to neural disruption in aMCI patients.

Memory and Other Cognitive Processes

September 20, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Memory is involved in all cognitive processes. Neuroscience is a new emerging, field and the research into other cognitive processes is just beginning. Much further research is needed before it is ready for public consumption.

The few definitive facts on this topic appear in the Chapter Summary, which follow:

“*Visual attention increases activity in visual sensory regions and is also associated with activity in dorsolateral prefrontal cortex and parietal cortex control regions.

Visual working memory is associated with the same sensory regions and control regions associated with attention, which likely reflects attention to the contents of working memory.

*Visual long-term memory is associated with the same regions associated with visual attention in addition to the medial temporal lobe, which indicates this cognitive priocess is distinct from attention.

*Imagery and working memory share the same cognitive operations and are associated with the same brain regions (i.e., the sensory cortex, the dorsolateral prefrontal cortex (i.e., Broca’s area) and the left posterior superior temporal cortex (i.e., Wernicke’s area).

*Memory for emotional information is thought to be enhanced through the interaction of the amygdala and the hippocampus.”

False Memories

September 19, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

False memories often stem from memory for the general theme of previous events, called gist. The Deese-Roediger-McDermott (DRM) paradigm is commonly used to study false memory. In the DRM paradigm, lists of associated words are presented during the study phase (e.g.,”web’, ‘insect’, ‘fly’,) and then during the test phase old words, new related words (e.g., ‘spider’), and new unrelated words are presented and participants make “old” — “new” recognition judgments. Not surprisingly, participants have very high levels of false memories for new related words in these paradigms (they usually respond “old” to “spider” in the example above). It is thought that when the associated words are presented during the study phase in such paradigms, participants learn the gist of the list, and this leads to a false memory for the related item. Schacter and others have argued that remembering gist is an important feature of our memory system. Memory for gist is useful as it allows us to remember general information without getting bogged down by useless details. For example, when a person sees a friend (or an enemy) it makes more sense for them to remember the gist of that person rather than retrieve all of their previous interactions. The brain regions associated with true memory and gist-based false memories are very similar.

There are differences in brain activity between true memory and false memory. There was greater activity for true memory than false memory in more posterior early visual processing regions, including V1. These findings indicate that activity in early sensory regions can distinguish between true memory and false memory. The same pattern of visual area activity was reported in a subsequent study that used words as stimuli. So the question is if early visual regions can distinguish between true memory and false memory, why don’t participants use this information to respond “new” to related items? Slotnick and Schacter reasoned that if participants had conscious access to this information they would have used it to correctly reject new related items and, therefore, activity in early visual processing regions may reflect non consciousness. So our conscious mind remains ignorant of what our brain could tell us.

This research is important for neuroscience. However, the research on false memories in the cognitive literature is highly relevant to the law and legal issues. False memories have lead to the wrongful conviction and imprisonment of too many individuals. And there is ample research showing how false memories can be implanted into our brains. The leading researcher in this area is Elizabeth Loftus. Entering “Loftus” into the search box of the healthy memory blog will locate ten posts describing her research.
This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

False memories often stem from memory for the general theme of previous events, called gist. The Deese-Roediger-McDermott (DRM) paradigm is commonly used to study false memory. In the DRM paradigm, lists of associated words are presented during the study phase (e.g.,”web’, ‘insect’, ‘fly’,) and then during the test phase old words, new related words (e.g., ‘spider’), and new unrelated words are presented and participants make “old” — “new” recognition judgments. Not surprisingly, participants have very high levels of false memories for new related words in these paradigms (they usually respond “old” to “spider” in the example above). It is thought that when the associated words are presented during the study phase in such paradigms, participants learn the gist of the list, and this leads to a false memory for the related item. Schacter and others have argued that remembering gist is an important feature of our memory system. Memory for gist is useful as it allows us to remember general information without getting bogged down by useless details. For example, when a person sees a friend (or an enemy) it makes more sense for them to remember the gist of that person rather than retrieve all of their previous interactions. The brain regions associated with true memory and gist-based false memories are very similar.

There are differences in brain activity between true memory and false memory. There was greater activity for true memory than false memory in more posterior early visual processing regions, including V1. These findings indicate that activity in early sensory regions can distinguish between true memory and false memory. The same pattern of visual area activity was reported in a subsequent study that used words as stimuli. So the question is if early visual regions can distinguish between true memory and false memory, why don’t participants use this information to respond “new” to related items? Slotnick and Schacter reasoned that if participants had conscious access to this information they would have used it to correctly reject new related items and, therefore, activity in early visual processing regions may reflect non consciousness. So our conscious mind remains ignorant of what our brain could tell us.

This research is important for neuroscience. However, the research on false memories in the cognitive literature is highly relevant to the law and legal issues. False memories have lead to the wrongful conviction and imprisonment of too many individuals. And there is ample research showing how false memories can be implanted into our brains. The leading researcher in this area is Elizabeth Loftus. Entering “Loftus” into the search box of the healthy memory blog will locate ten posts describing her research.

Motivated Forgetting

September 18, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Like retrieval-induced forgetting, motivated forgetting refers to an active process where retrieval of an item from memory is suppressed. Unlike retrieval-induced forgetting process, motivated forgetting is an intentional process.

So the research paradigm is obvious, present lists of words where words are designated to be remembered or forgotten. But the behavioral results of such an experiment would be obvious, and many would wonder why the study was done. Participants simply ignored the words designated to be forgotten and would study the words to be remembered.

Although a simple behavioral experiment would be silly, the same experiment measuring brain regions would be informative. The first study that investigated the brain regions associated with motivated forgetting employed fMRI. During the study phase, pairs of words were presented. During the think/no think phase, the initial words of some pairs were shown in red, which meant the associated word should not be thought about. The initial words of some pairs were shown in green, which meant that the associated word should be rehearsed. The initial words of some pairs were not shown, which served as a baseline measure of memory performance. During the final recall phase, all of the initial words pairs were shown.

The percentage of associated words recalled in the no-think condition was lower than the percentage of associated words recalled in the baseline condition, which reflected motivated forgetting. The percentage of associate words recalled in the think condition was higher than baseline performance, which was expected due to additional rehearsal.

Brain activity associated with motivated forgetting was identified by contrasting non-think trials (which were assisted with subsequent forgetting) and think trials (which were not associated with subsequent forgetting). Motivated forgetting was associated with an increase in activity within the dorsolateral prefrontal cortex and a decrease of activity in the hippocampus.

A literature review has shown that motivated forgetting consistently produces an increase in activity within the dorsolateral prefrontal cortex and a decrease of activity within the hippocampus. In addition, motivated forgetting of visual information produces a decrease in activity within the visual sensory regions. This overall pattern of brain activity during motivated forgetting is identical to that of retrieval-induced forgetting. These findings provide convergent evidence that active forgetting, whether retrieval-based or motivated, is cause by a top-down signal within the dorsolateral prefrontal cortex that inhibits the hippocampus and sensory cortical regions.

Retrieval-Induced Forgetting

September 17, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Retrieval-induced is an active process where retrieval of an item from memory inhibits the retrieval of related words. For example, if the word “banana” is recalled, the memory representation of the related word “orange,” which is also a fruit, will be inhibited to some degree. Presumably such inhibition occurs to reduce the likelihood that a similar but incorrect item will be retrieved (to avoid mistakenly saying “orange” when one intends to say “banana.”)

The paradigm used to study retrieval-induced forgetting includes an initial study phase, an intermediate retrieval practice, and a final recall phase. In one fMRI experiment, participants were presented with word pairs consisting of a category and an example of the category in the study phase. During the intermediate retrieval practice phase, participants were presented with a subset of the categories along with a two-letter word cue and were asked to mentally complete each word (during this phase, non-presented words from the same categories were inhibited). In the final recall phase, participants were presented with all of the categories and word cues corresponding to the word pairs from the study phase. Categories/words that were presented in the study phase but were not presented in the retrieval practice served as a baseline level of performance (since these words were not inhibited.) Retrieval-induced forgetting was revealed as a lower percentage of recall for words that were from the same category than the percentage of recall for words that were from a different category that were not presented during retrieval practice.

To identify brain regions associated with retrieval-induced forgetting during the final recall phase, non-presented words from the same category as those presented during retrieval practice (which were inhibited) were compared with practice words (which were not inhibited). This contrast produced activity in the dorsolateral prefrontal cortex. The larger the magnitude of activity in the dorsolateral prefrontal cortex, the higher the percentage of retrieval-induced forgetting. This suggests that the dorsolateral prefrontal cortex actively inhibits non-presented words from the same category as words presented during retrieval practice.

Another retrieval-induced forgetting study used transcranial direct current stimulation (tDCS) to disrupt activity in the right dorsolateral prefrontal cortex during the practice phase. This completely eliminated the retrieval-induced forgetting effect, indicating that the dorsolateral prefrontal cortex is necessary to produce this type of forgetting.

Typical Forgetting

September 16, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Usually forgetting in everyday life can be attributed to a failure to attend to information. One might not be interested in the material, distracted by a cell phone, been sleepy, or thinking about something else. Attention is key to remembering and not forgetting. If participants are asked to deeply process words, such as deciding whether each word in a study list is “pleasant” or “unpleasant,” their memory performance will be similar whether or not they knew there is a subsequent memory test. Successfully encoding information requires attention rather than the knowledge that the information will be tested at a later time.

The pattern of brain activity associated with subsequent forgetting is the same as the pattern of brain activity that is referred to as the default network. The default network consists of the regions of the brain that become active when participants are not engaged in any particular task, such as when they lay quietly with their eyes closed, passively looking at a fixation point on the screen, or waiting between experimental trials. This network of brain activity has been associated with many cognitive states, such as daydreaming, mind wandering, lapses of attention, and retrieval of personal information.

So in the real world one knows to minimize distractions and attend to information that is important. To avoid forgetting, one needs to focus attention and stay engaged. So minimize multitasking. Staying constantly plugged in guarantees superficial understanding.

Phase and Frequency of Activity Associated with Long Term Memory

September 15, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Frequency refers to the rate of change in magnitude over time. Frequencies can be low, changing slowly over time, or high, changing rapidly over time. Brain activity time courses can be considered from a frequency perspective, with lower frequencies corresponding to slower changes in signal over time, and higher frequencies corresponding to the faster changes in signal over time. Certain frequencies of brain activity have been associated with memory and have been linked to particular brain regions. Specifically, memory has been associated with brain activity that oscillates in the theta frequency band (4 to 8 Hertz), the alpha frequency band (8 to 12 Hertz) and the gamma frequency band (greater than 30 Hertz). In the fields of visual perception and visual attention, gamma activity is known to reflect binding of features that are processed in different cortical regions (such as shape and color). Gamma activity is a mechanism that underlies the perception of unified objects. Theta activity (4 to 8 Hertz) reflects the interaction the hippocampus and cortical regions have during long-term memory, and alpha activity reflects cortical inhibition.

In addition to modulation of activity within theta, alpha, and gamma frequency bands during memory, there is evidence that brain regions with different frequencies of modulation can be in phase with each other. This is called cross-frequency coupling and indicates two brain regions interact. In a long-term memory electroencephalography (EEG) study, participants viewed picture of objects during the study phase and then during the test phase were presented with old and new pictures of objects and made “remember’ “new” judgments. Subsequently remembered items as compared to subsequently forgotten items were associated with an increase in beta activity in right frontal regions, a decrease in alpha activity in anterior and posterior regions, and an increase in gamma activity in parietal and occipital regions (from 300 to 1300 milliseconds after stimulus onset). Moreover, there was greater cross-frequency coupling for subsequently remembered than subsequently forgotten items between frontal theta activity and parietal-occipital gamma activity. The identical pattern of results for theta activity and gamma activity was observed with the same experimental protocol during memory retrieval. Based on the known role of gamma activity in visual perception and attention, it can be assumed that the increase in parietal-occipital gamma activity in these studies reflected an increase in visual object processing associated with remembered items, and frontal theta activity may have modulated the gamma activity. Of special importance, the cross-frequency coupling evidence suggests that frontal regions and parietal-occipital regions interacted during long-term memory encoding and retrieval.

To summarize succinctly, theta activity reflects the interaction between the hippocampus and cortical regions during long-term memory, alpha activity reflects cortical inhibition, and gamma activity reflects process of features in different cortical regions that are combined to create a unified memory.

Superior Long Term Memory

September 14, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Perhaps the most famous research on superior memory, one that has been reported in previous healthy memory blog posts regards London taxi drivers. At one time they needed to memorize the layout of 25,000 city streets and the locations of thousands of city attractions. One study investigated whether there were differences in the size of brain regions between taxi drivers and control participants. They found that these taxi drivers had changes in the size of only their hippocampus, with a relative increase in the amount of gray matter within the posterior hippocampus and a relative decrease in the amount of gray matter within the anterior hippocampus. Moreover, the types changes in both types of hippocampal gray matter size correlated with the length of time they had been taxi drivers, which ranged from 1.5 to 52 years (with the largest changes for those who had been taxi drivers the longest).

A follow-up study compared the brain region sizes between London taxi drivers and London bus drivers, who were a better matched control in terms of driving experience, stress, and other factors. The same results were obtained, where the taxi drivers had a relatively larger posterior hippocampus and a relatively smaller anterior hippocampus than bus drivers, and this correlated with the length of time they had been driving a taxi.

Another group of people who have superior memory are those who participate in the World Memory Championships and those who are known for extraordinary memory abilities. A study compared such individuals with control participants to asses whether there were differences in cognitive abilities, differences in the size of brain regions, and differences in the magnitude of fMRI activation during memory tasks. People defined as having superior memory did not differ from control participants in the cognitive abilities tested (IQ ranges were 95 to 119 and 98 to 119, respectively) or in the size of an brain regions. The fMRI task required superior memory for a sequence of digits (a task where those whose superior memory excelled), memory for a sequence of faces, or memory for a sequence of snowflakes. Across tasks, those with superior memory had greater activation in the posterior hippocampus, the retrosplenial cortex, and the medial parietal cortex, which are regions that have been associated with long term memory. Almost all of the participants with superior memory reported using a memory strategy called the method of loci. (entering method of loci into the search block of the healthy memory blog yields 11 hits).

Another case study investigated another individual with a superior memory, who is known as PI, was able to recall the digits of pi to more than 65,000 decimal places. His performance was similar to control participants on the large majority of cognitive tasks. Not surprisingly his working memory was in the 99.9th percentile. But it is conceivable that that might be the result of the extraordinary amount of time he spent memorizing pi. His general memory was average. He was impaired on test of visual memory (3rd percentile or below).

He also reports on individuals who are considered as having highly superior autobiographical memory or HSAMers. There have been eight previous posts on HSAMers. These are people who have detailed episodic memory for every day of their later childhood and adult life. If they are given any date, they can recall the day of the week, and public events that occurred on that day of the week. In one study of HSAMers their performance was normal on most standard cognitive tasks. A comparison of different brain regions between HSAMers and control participants revealed a number of differences including greater white matter coherence in the parahippocampal gyrus, which could reflect greater contextual processing associated with episodic retrieval, and a relatively smaller anterior temporal cortex. The decrease in size of the anterior temporal cortex, which has been associated with semantic memory, may reflect the disuse of this region because those with HSAM rely more on episodic retrieval. Much more research needs to be done with this interesting group.

Sex Differences in Long Term Memory

September 13, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Males usually perform better on navigating previously learned environment. Females usually perform better on long-term memory tasks that can depend on verbal memory such as word list recognition and recall, associative memory, and autobiographical memory. Since almost all long-term memory tasks can be performed using verbal memory strategies, females generally have better behavioral performance than males. Females have larger numbers of estrogen receptors in the hippocampus and dorsolateral prefrontal cortex. These are two of the three regions associated with long-term memory, which can increase the activity of these regions. The hippocampus and the dorsolateral prefrontal cortex are larger in females than males, relative to overall brain size. Additionally, females have relatively larger volumes of language processing cortex, which likely contributes to their superior verbal memory.

In addition, females and males often employ different cognitive strategies and have distinct patterns of brain activity while they perform the same task. An fMRI study investigated whether there were sex differences in the hippocampus during memory for object-location associations. There were 10 female and 10 male participants. During study blocks, participants viewed a video as if they were walking through a virtual environment with five colored geometric objects. During recognition blocks, an aerial view of each object was shown in a old location or a new location. Participants responded whether each was in an “old” or “new” location. Each participant also used a four-point rating scale to describe the strategy they used to learn the object locations: (1) completely verbal, (2) more verbal than pictorial, (3) more pictorial than verbal, and (4) completely pictorial.

Although there was no difference in behavioral performance between female participants and male participants, the average strategy for female participants was 2.5 and the average strategy rating for male participants was 4.0 indicating that female participants employed more verbal memory strategies and male participants employed purely spatial/non-verbal strategies. The fMRI data indicated that activity was localized to the left hippocampus in the large majority of female participants and that activity was localize to the right hippocampus in the large majority of male participants. These results are consistent with patient studies indicating the lesions in the left medial temporal lobe impair verbal memory and lesions in the right medial temporal lobe impair visual memory.

Long Term Memory Consolidation and Sleep

September 12, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

It appears that a primary role of sleep is to integrate new memories into our vast memory store with the minimal disruption of old memories. Sleep involves rapid eye movements (REM) periods and non-REM periods that alternate every ninety minutes, with four stages of progressively deeper non-REM sleep. The first half of a night’s sleep is dominated by non-REM sleep, while the amount of REM sleep increases during the second half of the night. Non-REM stages 3 and 4, referred to as slow wave sleep, are of special relevance because these periods are important for consolidation of long-term memories. REM sleep seems to be particularly important for consolidation of implicit memories.

Slow wave sleep is associated with slow (less than 1 Hertz) waves of brain activity that are measured across the entire scalp using EEG. The slow waves orchestrate a number of brain processes that mediate the process of long-term memory consolidation. Slow waves alternate between down-states corresponding to global decreases in brain activity and upstates corresponding to global increases in brain activity. Slow waves synchronize other brain waves including thalamic-cortical sleep spindles (that oscillate at frequencies of 11-16 Hertz) and hippocampal sharp-wave ripples (that oscillate at a frequency of approximately 200 Hertz). Hippocampal sharp-wave ripples are of particular importance as they are known to coordinate the hippocampal-cortical interactions that reflect the reproduction of memories from the previous waking period. In brief, important long term memories from the previous waking period are replayed during slow wave sleep, which in turn strengthens these memories and results in consolidation. Although this mechanism for memory consolidation is based on strengthening of memory representations through repeated activations, it has been proposed that sleep may also weaken memory representation of unimportant events to provide a clean slate for next day’s events. It is interesting to note that Dr. Slotnick dedicates this book to his incredible daughter Sonya, for dominating my hippocampal sharp-wave spindles these past twelve years. This section should convince all readers that all-nighters are not only fruitless, but also counterproductive. One wants to have memories well-consolidated prior to taking an exam.

Brain Regions Associated with Long-Term Memory

September 11, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Dr. Slotnick writes, The term episodic memory can refer to many other related forms of memory including context memory, source memory, “remembering,” recollection, and autobiographical memory, which refers to a specific type of episodic memory for detailed personal events. As the names imply context memory and source memory refer to the context in which something occurred and source memory refers to where the event occurred.

Episodic memories are related to activity in both control regions and sensory regions of the brain. Sensory cortical activity reflects the contents of memory. The control regions that mediate episodic memory include the medial temporal lobe, the dorsolateral prefrontal cortex, and the parietal cortex. There are many regions associated with episodic memory but the primary regions are the medial temporal lobe, the dorsolateral prefrontal cortex, and the parietal cortex. The parahippocampal cortex processes the context of previously presented information such as the location or the color.

The hippocampus binds item information and context information to create a detailed episodic memory. Dr. Slotnick provides the following example. “If an individual went on a vacation to Newport Beach in California and later recalled meeting a friend on the beach, that individual’s perirhinal cortex would process item information (the friend), the parahippocampal cortex would process context information (the area of the beach on which they were standing), and the hippocampus would bind this information and context information into unified memory.”

Semantic memory refers to knowledge of facts that are learned through repeated exposure over a long period of time. These facts are processed and organized in semantic memory, which provides the basis for much thought. Subjectively, semantic memory is associated with “knowing.” Semantic memory includes definitions and conceptual knowledge, and this cognitive process is linked to the field of language.

Semantic memory has been associated with the left dorsolateral prefrontal cortex (in a different region associated with episodic memory), the anterior temporal lobes, and sensory cortical regions. The left dorsolateral prefrontal cortex may reflect the processing of selecting a semantic memory that is stored in other cortical memories. For example, naming animals activates more lateral inferior occipital-temporal cortex that has been associated with the perception of living things, while naming tools activates more medial inferior occipital-cortex that has been associated with perception of nonliving things.

In a study of Alzheimer’s patients, the impairment in an object naming task, which depends on intact semantic memory, was more highly correlated with cortical thinning in the left anterior temporal lobe. This finding suggests that the left anterior temporal lobe is necessary for semantic memory.

During long-term memory the hippocampus binds information between different cortical regions. But long-term memory may only depend on the hippocampus for a limited time. In the standard model of memory consolidation, a long-term memory representation changes from being based on hippocampal-cortical interactions to being based on cortical-cortical interaction, which takes a period of somewhere between 1 to 10 years. A person with hippocampal damage due to a temporary lack of oxygen might have impaired long-term memory for approximately 1 year before the time of damage from retrograde amnesia and have intact long-term memories for earlier events. This suggests that the hippocampus is involved in long-term memory retrieval for approximately 1year as more remote long-term memories no longer demand on the hippocampus so they are not disrupted.

The activity in the hippocampus did not drop to zero for older semantic memories but was well above baseline for events that were 30 years old. This indicates that the hippocampus was involved in memory retrieval for this entire period. If the hippocampus was no longer involved, the magnitude of activity in this regions would have dropped to zero for remote memories.

There is a growing body of evidence that the hippocampus is involved in long-term memories throughout the lifetime. As such, the process of consolidation does not appear to result in the complete transfer from hippocampus-cortical memory representation to cortical-cortical memory representations.

Tools of Cognitive Neuroscience

September 10, 2019

The title of this post is identical to a chapter title in an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” The tools of cognitive neuroscience are highly technical. If the reader is interested in these techniques she should read Dr.Slotnick’s book, or look up the tools of interest in the Wikipedia.

One of the earliest techniques was positron emission tomography (PET). It required that a low level of radioactive material be injected into the participants bloodstream. This technique measured increased blood flow to the portions of the brain being activated. Fortunately a new technique that measured blood flow was found that did not require the injection of radioactive dye or any other type of material.

That technique was functional magnetic resonance imaging (fMRI), which also measured where in the brain the blood flow was increasing.

Event-related potentials (ERPs) can track brain activity in real time. ERPs directly measure neural activity and have a temporal resolution in milliseconds. Its spatial resolution is in centimeters, which is much lower than fMRI.

Electroencephalography (EEG) uses the identical data acquisition as ERPs, but refers to any measure of brain activity that corresponds to electric fields. This includes ERPs, but more commonly refers to brain activity that oscillates within a specific range of frequencies. EEG frequency analysis is a powerful alternative to the more commonly employed ERP analysis. Related to EEG, magnetoencephalography (MEG) refers to any measure of brain activity that corresponds to magnetic fields, and also typically refers to brain activity that oscillates within a specific frequency range. Like ERPs that are generated by averaging all the events of a given type from EEG data during a cognitive task, event-related fields (ERFs) are generated by averaging all the events of a given type from MEG data. The more general terms EEG and MEG also refer to ERPs and ERFs.

Dr. Slotnick writes, “fMRI is by far the most popular method in the field of cognitive neuroscience. However, brain activity is not a static set of blobs that represent a cognitive process. Rather, brain activity changes across different regions in milliseconds. Only techniques with excellent temporal resolution, such as ERPs, can track the functioning brain. This book highlights the temporal dimension of brain processing in addition to the spatial dimension of brain processing. One major advantage of temporal information is that one can use it to assess whether different brain regions are synchronously active, which indicates that these regions interact. This reflects how the brain is actually operating.”

Transcranial magnetic stimulation (TMS) can be used to temporarily disrupt processing in one region of the brain.

Transcranial direct current stimulation (tDCS) is similar to TMS in that it temp[orarily modulates processing in a target cortical region by stimulating with a weak direct current rather than a magnetic field.

A relatively new method called transcranial alternating current stimulation (tACS) uses the identical setup as tDCS, but the current alternatives at a specific frequency; this, tACS can stimulate the brain at a desired frequency.

Do not let yourself be discouraged or turned off by this technical stuff, but brief explanations are needed as these are the tools used in this research. The remainder of the posts will be on memory performance and on the portions of the brain contributing to this performance.

Sensory Reactivation Hypothesis

September 9, 2019

This post is based on information in an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” The sensory reactivation hypothesis states that memory for an event can activate the same brain regions associated with the perception of that event. These sensory memory effects reflect the contents of memory for a visual experience containing visual information.

There is a large body of research supporting the memory sensory reactivation hypothesis. Memory for visual information, language information (sounds or words), movement information (actions, and olfactory information reactivate the corresponding regions of the brain.) Within the visual process regions, there is also evidence that memory for faces and houses activate the fusiform face area (FFA) and the parahippocampal place area (PPA), respectively.

Evidence has also accumulated that memory for specific features activate the corresponding feature processing brain region. Memory for shape activates the lateral occipital complex (LOC), memory for colors activates V8, memory for items in the left visual field or right visual field activate the extra striate cortex in the opposite/contralateral hemisphere, and memory for motion activates region MT.

The concept of mental practice is relevant here. Athletes or performers mentally rehearse the activities they will need to perform. This mental rehearsal activates the relevant brain areas and the communications that need to be made to perform these activities. And this mental practice has beneficial effects on performance.

This is good to keep in mind if the weather or other complications preclude regular practice. Idle moments can be filled with mental rehearsal to make best use of one’s time.

Similarly one can use this sensory reactivation to re-experience pleasant experiences, be it an view, vacation highlights, sporting events, enjoyable meals. One can get maximum value for one’s entertainment dollar in this manner.

Brain Anatomy

September 8, 2019

The title of this post is identical to the title of a section in an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Brain Anatomy is a difficult topic to cover in a blog. The names can be learned and one can impress one’s friends and neighbors by reciting these names with their associated function. But the brain is a three dimensional structure and it is difficult illustrating these structures in two dimensions, especially since the position from which the brain is viewed is important. What is needed is a three dimensional model that can be rotated. Such a model can be found at http://www.brainfacts.org. Look for 3D Brain and click interact with the brain. It will likely take some practice interacting with the brain, but HM thinks this is the best source for this feature.

The brain is composed of four lobes: occipital, temporal, parietal, and frontal. Each lobe has gray matter on the surface, which primarily consists of cell bodies, and white matter below the surface, which primarily consists of cell axons that connect different cortical regions. The occipital lobe is associated with visual processing. The temporal lobe is associated with visual processing and language processing. The parietal lobe is associated with visual processing and attention, and the frontal lobe is associated with many cognitive processes. You can see that over half of the human brain is associated with visual processing. Obviously we are primarily visual animals.

The regions of the brain that are of relevance to memory include the occipital cortex, the temporal cortex, the parietal cortex, the dorsolateral prefrontal cortex, and the medial temporal lobe. The cortex is folded with gyri protruding out and sulk folding in.

The hippocampus (you can look for this using the link provided above) is a structure central to long-term memory. Its importance was realized when surgery was done on a patient, H.M., done to treat the severe epileptic seizures he was having. The medial temporal lobe, which contains the hippocampus, was removed in both hemispheres. This surgery did not affect his intelligence or personality, but it did cause a severe deficit in long-term memory referred to as amnesia. His semantic memory remained intact. He had almost no memory of events that occurred a few years before the surgery, and had no memory for events that occurred after the surgery. Ten months before the surgery he and his family moved to a new house a few blocks away from their old house. After the surgery he had no memory for his new address, he could not find his way to the new home, and he did not know where objects were kept in the new home. He had no memory of articles he had read before, so he would read the same articles repeatedly. He would eat lunch and a half-hour later could not remember he had eaten. Despite this severe deficit in long-term memory, his working memory appeared intact. He could remember a pair of words or a three-digit number for several minutes as long as he was not distracted. So a reasonable conclusion is that the hippocampus and the surrounding cortical regions are critical for long-term memory.

Dr. Slotnick writes, “Long-term memory typically refers to retrieval of previously presented information, However, the key stages of long-term memory include encoding, storage, and retrieval. The hippocampus has been associated with both long-term memory encoding and long-term memory retrieval. Long-term memory storage depends on a process called memory consolidation, which refers to changes in brain regions, including the hippocampus, underlying long-term memory. Thus, all three stages of long-term memory depend on the hippocampus.”

Sometimes people think of the hippocampus as being the location where long-term memories are stored. Memories are stored throughout the brain, it is the processing of these memories for which the hippocampus is critical.

The Role of Introspection

September 7, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” The initial research approach taken in the early days of psychology was introspection. As all humans can access their own minds, it seemed like an obvious approach, to simply record how humans are using their own minds. Reams of research were collected using this approach. But no theories or hypothesis emerged, nor were there techniques for testing hypotheses, which is central to all science. The result was a radical rejection of this subjective approach and the beginning of behaviorism, in which only observed behaviors were an appropriate source of data for psychologists.

Only recently has introspection been accepted back into rigorous psychological research. Introspection has been found useful in identifying which kind(s) of memory operated during a particular task.

The renowned psychologist Endel Tulving hypothesized that there was a distinction between “remembering” and “knowing.” Tulving recognized this distinction from his own introspections. But he did not stop there. There was research on a patient with a brain lesion who had no detailed memory of the past (he could not remember) but still could define words. Tulving designed and ran experiments to test the hypothesis that “remember” responses and “know” responses were distinct. During one experiment, words were presented during the study phase, and then during the test phase old words and new words were presented and participants made “old” and “new” recognition judgments. For old items correctly classified as “old,” participants also made a “remember” – “know” judgment and a confidence-rating judgment (ranging from 1 to 3 corresponding to low confidence, intermediate confidence, and high confidence). The probability of “remember” responses increased with increasing confidence, while the probability of “know” responses was maximal at the intermediate confidence rating.

These distinct response profiles provide behavioral evidence in support of Tulving’s hypotheses that “remembering” and “knowing” are distinct types of memory. This research is strictly cognitive psychology. However, a large body of research in cognitive neuroscience has subsequently accumulated showing that “remembering” and “knowing” are also associated with distinct regions of the brain.

Alzheimer’s Researchers Shift Focus After Failures

July 7, 2019

The title of this post is identical to the title of a front page article by Christopher Rowland in the 4 July 2019 issue of the Washington Post. These researchers are shifting their focus to new drug treatments that deal with other factors than the defining features for an Alzheimer’s diagnose, which are amyloid plaque and neurofibrillary tangles. The conclusion that this research is fruitless was made by a former researcher in this area. The Myth of Alzheimer’s is a book by Peter J. Whitehouse, M.D. and Ph.D and Daniel George, M.Sc. Whitehouse is the former researcher who came to the conclusion that this research would never yield results. There was a healthy memory post on this book in 2011. HM believes Dr. Whitehouse is working on non drug treatments for Alzheimer’s. The Alzheimer’s association provides little, if any, support in this area. The Alzheimer’s association provides financial support for drug research. HM wonders in the unlikely event that a useful drug was produced, whether the Alzheimer’s Association had some agreement to limit costs or would this company be allowed to prey on the public. Before giving any money to the Alzheimer’s association, potential donors should demand an answer to this question.

There have been many posts on this topic including one titled “The Myth of Alzheimer’s.” Perhaps the most significant finding is one that is rarely, if ever, mentioned. And that is that people die with the defining characteristics for an Alzheimer’s diagnosis, the amyloid plaque and neurofibrillary tangles, but who never knew that they had the disease because they never had any behavioral or cognitive symptoms of the disease. The explanation offered is that these people had developed a cognitive reserve as a result of being cognitively active during their lifetimes.

The reappearing theme in this blog is that people should live cognitively fulfilling lives with growth mindsets in which they are continuing to learn. This involves System 2 processing, more commonly referred to as thinking. Our normal processing mode is System 1, which is quite fast and efficient. Here we are in cruise control where the conscious content just keeps flowing. As one proceeds through life this becomes easier and easier. Much has been learned, there is little interest in learning anything new, so the mind effectively is on cruise control. Cognitive neuroscience has termed this the default mode network, which is quite similar, if not identical, to Kahneman’s System 2 processing which is from cognitive psychology.

HM knows people who have been cognitively active throughout their lives, yet still succumbed to Alzheimer’s or dementia. But there are other causes. One of HM’s friends trained himself to get by on 4 hours of sleep per night. Research shows us that 7 to 8 hours of sleep are required. Other ambitious people burn the candle and both ends, which also leads to sleep deprivation.

HM wishes the researchers well in their research. But everyone should know that by engaging in a cognitively challenging life with growth mindsets they should greatly decrease, if not eliminate, the prospect of dementia or Alzheimer’s. Of course, a healthy lifestyle is also assumed.

Please use the search block of the blog (healthymemory.wordpress.com) to learn more about any of the terms in this post.

© Douglas Griffith and healthymemory.wordpress.com, 2019. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Default Network, System 1 Processing, and Alzheimer’s Disease (AD)

May 8, 2019

An earlier healthy memory blog post promised more about the default mode network. That post identified similarities between the default mode network and Kahneman’s System 1 Processing. Kahneman’s System 1 processing is important in that HM thinks that too heavy a use of System 1 processing at the expense of System 2 processing, which is active thinking, increases the risk for AD.

The simplest distinction between the two terms is that Kahneman is a cognitive psychologist and his two process view of of cognitive processes comes from cognitive psychology. The default mode network comes from cognitive neuroscience. Default mode activity is identified via brain imaging. Although they might not be identical, that distinction awaits further research, it is clear that there is considerable overlap between the two.

In addition to brain atrophy, AD patients have abnormal high levels of proteins in different brain regions. In the medial temporal lobe, the accumulation of tau protein leads to neurofibrillary tangles. In cortical regions, such as the parietal cortex in early AD, the accumulation of amyloid-B protein leads to amyloid plaques. The neurofibrillary tangles in the medial temporal lobe and amyloid plaques in cortical regions can be assumed to disrupt neural processing in these regions.

Dr. Slotnick writes, “There is an influential hypothesis that were is a causal relationship between default network activity that leads to deposition of amyloid that results in atrophy and disrupted metabolic activity, which impairs long-term memory in AD patients. The regions in the default network are active when participants are not engaged in a task and include the dorsolateral prefrontal cortex, the medial prefrontal cortex, the inferior prefrontal cortex and the medial parietal cortex. In AD patients, amyloid deposition occurs in the same regions, which suggests the default network activity may lead to amyloid deposition. Dr. Slotnick suggests that perhaps higher level of amyloid deposition, which occurs in late AD patients, is necessary to produce atrophy in the frontal cortex.

Dr. Slotnick continues, “If high amyloid deposition is a causal factor in developing AD, older adults with low levels of amyloid should be at decreased risk for developing this disease. There is some evidence that cognitive engagement and exercise engagement throughout life may reduce the amyloid level in the brains of healthy older adults as a function of cognitive engagement, and this was compared to the cortical amyloid levels . Participants rated the frequency which they engaged in cognitively demanding tasks such as reading, writing, going to the library, or playing games at five different ages (6, 12, 18, 40, and their current age). Healthy older adults with greater cognitive engagement throughout their lifetime, as measured by the average cognitive activity at the five ages, had lower levels of amyloid in default network regions. Moreover, the healthy older adults in the lowest one-third of lifetime engagement had amyloid levels that were equivalent to AD patients, and the healthy older adults in the highest one-third of lifetime cognitive engagement had amyloid levels that were equivalent to young adults.

So maintaining a growth mindset, thinking critically, and learning new information provide double protection against AD. First, the reduction of troublesome amyloid levels. Second is the building of a cognitive reserve so that even if you develop amyloid plaque and neurofibrillary tangles you may not have the cognitive and behavior symptoms of AD.

Dr. Slotnick’s work is reported in an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” The report on which Dr. Slotnick’s statements are based comes from
Buckner, R.L., Snyder, A.Z., Shannon, B.J., LaRossa, G. Sachs, R. Fotenos, A.F., Sheline, Y.I., Klunk, W.E., Mathis, C.A., Morris, J.C. & Mintun, M.A. (2005). Molecular, structural, and functional characterization of Alzheimer’s disease: Evidence for a relationship between default activity, amyloid, and memory. The Journal of Neuroscience, 25, 7709-7717.

© Douglas Griffith and healthymemory.wordpress.com, 2019. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

Passing 73

May 6, 2019

Meaning that today HM is entering his 74th year. He engages in ikigai, the Japanese term referring to living a life with purpose, a meaningful life. His purpose, in addition to living a fulfilling life with his wife, is to learn and share his thoughts and knowledge with others. HM does this primarily through his blog healthymemory, which focuses on memory health and technology.

HM’s Ph.D is in cognitive psychology. That field has transitioned to cognitive neuroscience, a field of research and a term that did not exist when HM was awarded his Ph.D. HM is envious of today’s students. However, he is still fortunate enough to be able to keep abreast of current research and to relay relevant and meaningful research from this field to his readers.

What is most disturbing is the atmosphere of fear and hate that prevails today. It is ironic that technology, which had, and still has, a tremendous potential for spreading knowledge, now largely spreads disinformation, hatred, and fear.

HM understands why this is the case, but, unfortunately, he does not know how to counter it.

The problem can best be understood in terms of Kahneman’s Two Process Theory of cognition. In Nobel Lauerate Daniel Kahneman’s Two System View of Cognition. System 1, intuition, is our normal mode of processing and requires little or no attention. Unfortunately System 1 is largely governed by emotions. Fear and hate are System 1 processes. System 2, commonly referred to as thinking, requires our attention. One of the roles of System 2 is to monitor System 1. When we encounter something contradictory to what we believe, the brain sets off a distinct signal. It is easier to ignore this signal and to continue System 1 processing. To engage System 2 requires attentional resources to attempt to resolve the discrepancy and to seek further understanding. To put Kahneman’s ideas into the vernacular, System 2 involves thinking. System 1 is automatic and requires virtually no cognitive effort. Emotions are a System 1 process, as are identity based politics. Politics based on going with people who look like you requires no thinking yet provides social support.

Trump’s lying is ubiquitous. Odds are that anything he says is a lie. His entire candidacy was based on lies. So why is he popular? Identifying lies and correcting misinformation requires mental effort, System 2 processing. It is easier to be guided by emotions than to expend mental effort. The product of this cognitive miserliness is a stupidity pandemic.

Previous healthy memory posts have emphasized the enormous potential of technology. Today people, especially young people, are plugged in to their iPhones. Unfortunately, the end result is superficial processing. They get information expeditiously, but they are so consumed with staying in touch with updated information, that they have neither time nor attention left for meaningful System 2 processing. Unfortunately, technology, specifically social media, amplifies these bad effects, thus increasing misinformation, hatred and fear. Countering these bad effects requires implementing System 2 processes, that is thinking. A massive failure to do this enables Trump to build his politics on lies spreading hatred and fear.

As has been written in many previous healthy memory posts, System 2 processing will not only benefit politics, but will also decrease the probability of suffering from Alzheimer’s and dementia.

Personally, all this is upsetting. But HM believes it is essential to love one’s fellow humans. He tries to deal with this via meditation. Progress is both difficult and slow but it needs to be done. Hatred destroys the one who hates. So HM continues a daily struggle to be a better human being.

© Douglas Griffith and healthymemory.wordpress.com, 2019. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.

The Knowledge Illusion: Why We Never Think Alone (Unabridged)

July 1, 2017

“The Knowledge Illusion: Why We Never Think Alone” is an important book by Steven Sloman and Phillip Fernbach. An earlier healthy memory blog post with the same title as the book has already been written. That post was based on a summary of the book done by Elizabeth Kolbert for the New Yorker. Having now read the entire book, HM feels that this volume deserves more detailed attention.

Drs. Sloman and Fernbach are cognitive scientists. Cognitive science emerged in the 1950s to understand the workings of the human mind. It asks questions such as “how is thinking possible?” What goes on inside the brain that allows sentient beings to do math, understand their mortality, act virtuously and (sometimes) selflessly, and still do simple things, like eat with a knife and fork? Currently no machine, and probably no other animal, is capable of these acts.

The authors write, “The human mind is not like a desktop computer, designed to hold reams of information. The mind is a flexible problem solver that evolved to extract only the most useful information to guide decisions in new situations. As a consequence, we individuals store very little detailed information about the world in our heads. In that sense people are like bees and society a beehive: Our intelligence resides not in individual brains, but in the collective mind. To function, individuals rely not only on knowledge stored within our skulls, but also on knowledge stored elsewhere: in our bodies, in the environment, and especially in other people.” In the lingo of the healthy memory blog, information not held within our individual brains, is stored in transactive memory. The authors conclude, “When you put it all together, human thought thought is incredibly impressive, but it is a product of a community, not of any individual alone.”

The authors make a compelling argument that we all suffer, to a greater or lesser extent, from an illusion of understanding, an illusion that we understand how things work when in fact our understanding is meager. Unfortunately, we are not adequately aware of the shortcomings in our understanding. We think we understand much much more than we actually do. Readers of the healthy memory blog should be aware of the risks of having absolute beliefs, that all beliefs should be hedged with some reasonable degree of doubt.

The authors note that history is full of events that seem familiar, that elicit a sense of mild to deep understanding, but whose true historical context is different that we imagine. The complex details get lost in the mist of time while myths emerge that simplify and make stories digestible in part to service one interest group or another. There is a very interesting book by James W. Lowen titled “Lies My Teacher Told Me: Everything Your American History Textbook got wrong”. He argues that history as taught in the public schools is basically propaganda advanced by the school board selecting texts. HM found this book most instructive. People should be recalled for a defective education, but reading this book is more practical.

It is also important to remember that the study of history is dynamic. New research yields new interpretations of history.

The authors write, “Thought is for action. Thinking evolved as an extension of the ability to act effectively; it evolved to make us better at doing what’s necessary to achieve our goals. Thought allows us to select from among a set of possible actions by predicting the effects of each action and by imagining how the world would be if we had taken different actions in the past.”

It is unlikely that we would have survived had we been dependent on only the limited knowledge stored in our individual brains. The authors write,”The secret to our success is that we live in a world in which knowledge is all around us. It is in the things we make, in our bodies and workspaces, and another people. We live in a community of knowledge.”

But not all of this is knowledge is accurate, meaning that there are degrees of belief and some knowledge is faux. Understanding that our knowledge is not golden can offer us improved ways of approaching our most complex problems. Recognizing the limits of our understanding should make us more humble, and open our minds to other people’s ideas and ways of thinking. The authors note that It offers lessons about how to avoid things like bad financial decisions, and can enable us to improve our political system and help us assess how much reliance we should have on experts versus how much decision-making power should be given to individual voters.

The authors write, “This book is being written at a time of immense polarization on the American political scene. Liberals and conservative find each other’s views repugnant, and as a result, Democrats and Republicans cannot find common ground or compromise.” The authors note, “One reason for this gridlock is that both politicians and voters don’t realize how little they understand. Whenever an issue is important enough for public debate, it is also complicated enough to be difficult to understand.” They conclude, “Complexity abounds. If everybody understood this, our society would likely be less polarized.”

Neuroscience is much in the news as there have been many exciting developments in the field. Little is currently being written about cognitive science, although there are exciting and relevant new findings in cognitive science. The following is directly quoted from “The Knowledge Illusion: ”Our skulls may delimit the frontier of our brains, but they do not limit the frontier of our knowledge. The mind stretches beyond to include the body, the environment, and people other than one’s-self, so the study of the mind cannot be reduced to the study of the brain. Cognitive science is not the same as neuroscience.”

© Douglas Griffith and healthymemory.wordpress.com, 2017. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and healthymemory.wordpress.com with appropriate and specific direction to the original content.