Posts Tagged ‘Default network’

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.

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.

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.

An Important Part of the Brain Unknown to Most

November 30, 2013

That would be the precuneus. The precuneus is located on the inside of the brain between the two cerebral hemispheres in the rear region between the somatosensory cortex and forward of the visual cortex, which contains the cuneus. One of the reasons so few people are aware of the precuneus is that it has been difficult to study because it is difficult to access. Moreover, it is rarely subject to isolated injury due to strokes or trauma, such as gunshot wounds.

The precuneus appears to be a recently expanded part of the brain. It is poorly developed in the less developed primates such as New World monkeys. The human precuneus comprises a larger portion of the brain than in non-human primates or other animals. It has the most complex columnar organization and is among the last regions to myelinate.

Mental imagery regarding the self has been located in the forward part of the precuneus with the poster areas being involved in episodic memory. Episodic memory refers to events in our own personal lives. Another area of the precuneus has been linked to visuospatial imagery. Visuospatial imagery is central to many mnemonic techniques.

Functional imaging has linked the precuneus to processes involved in self-consciousness. This includes the important function of reflective self-awareness. For example, it would be involved in comparing ones own personality traits to those of other people.

Not surprisingly the precuneus is involved in many memory tasks, for example when people look at images and try to respond based on what they have remembered in regard to verbal questions about spatial details. It is also involved in source memories such as when you try to remember where you read a particular article or where you saw a particular person. It is believed that the precuneus is involved in a variety of processes in addition to episodic memory retrieval such as attention, working memory, and conscious attention.

One idea is that the precuneus, together with the posterior cingulate is pivotal for conscious information processing. The evidence for this idea comes from the effects of its disruption in epilepsy, brain lesions, and vegetative state. It is also thought that the ventral precuneus is involved with the default mode network, and that this involvement might underlie its role in self-consciousness.

As this research is fairly new some of these ideas should be regarded with caution. But even at this early state of research it is clear that the precuneus is important and and deserves to be more widely known.