Posts Tagged ‘medial temporal lobe’

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.

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.”

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.

The Hippocampus

May 18, 2017

The hippocampus receives considerable attention in “The Truth About Language” by Michael C. Corvallis.  As the hippocampus plays a critical role in memory, it is not surprising that it is central to language and time travel.  As we each have a hippocampus in each hemisphere of the brain, we have two hippocampi.

The importance of the hippocampus was first realized when an Englishman underwent surgery for epilepsy, and the surgery destroyed major parts of both hippocampi.  After this surgery he could no longer form new episodic memories.  Episodic memory involves memories having to do with the specific episodes of our lives.   Although his semantic memory, his general knowledge, remained intact.  Not only was he unable to recall the past, he was also incapable of imagining the future.

In the final years of my Mom’s life she suffered from dementia.  When I visited her, she was always glad to see me.  However, if an attendant took her to the restroom while I was visiting, when she returned she acted as if I had just arrived.  That is, she had stored no memory of my being there.

The hippocampus is the hub of the brain circuit involved in episodic memory and mental time travel.  Brain imaging shows it to be activated both when people remember past events and when they imagine possible future events.  It is also activated when people are asked to imagine purely fictitious  episodes.   Although other brain regions are involved, reflecting the fact that memory and imagination involve information stored in widely dispersed areas, the hippocampus appears to be the most critical component in that damage to it has the most debilitating effect on the ability to mentally escape the present.

The default-mode network, responsible for our mind wandering, is identifiable in primates and even in rats.  The hippocampus plays a critical role in both rat and human memory.  Recording from the hippocampus of the rat reveals that single neurons code where the animal is located in the spatial environment.  These neurons serve as place cells and together generate what has been termed a cognitive map of the environment that tells the rat where it is.  It plays the same role in humans.  Studies have shown that the hippocampus  is enlarged in licensed taxi drivers in London, who are required to memorize the map of London for their licenses.

Research using rats has indicated a similar competence.  In an experiment rats were trained to alternate left and right turns at a particular location in the maze.  Between trials they were introduced to a running wheel and, while they were running, activity in their hippocampi was recorded.  This activity coded which way the rats planned to turn in the maze on the next trial.  Apparently these rats were planning ahead for their next try at the maze.  The researchers also noted that autonomous activity in the hippocampus involved the computation of distances, and also supported the episodic recall of events and the planning of action sequences and goals.  One researcher wrote that “replay in the rat hippocampus can either lead or follow the behavior once the map of space is established.  This suggests that replay phenomena may support ‘mental time travel’ through the spatial map, both forward and backward in time.

Research on human patients about to undergo surgery had electrodes placed in cells in the medial temporal lobe, in an attempt to locate the source of epileptic seizures.  They were then asked to navigate a virtual town on a computer screen and to deliver items to one of the stores in the town.  Then were asked to recall only the items and not the location to which they were delivered.  However, the act of recall activated the place cells corresponding to that location, effectively mirroring the replay of place cells in the rat brain.

In another study, people were shown sequences of four videos of different events.  At one level. narratives were linked to each video, encouraging attention to individual details. At the next level, narratives linked a par of videos, and at the final level a narrative linked all four videos.  As the people processed these narratives, activation in the hippocampus progressed from the rearward end to the forward end as the scale of the narrative shifted from small and detailed to larger and more global.    Dr. Corvallis notes that this probably happens when we read novels.  Page by page, we focus on the details, but as the story progresses we build a more global understanding of what the story is about.  Dr. Corvallis writes, be thankful to your hippocampi that you can make sense of a novel at all.

Dr. Corvallis suggests that although  the generativity spatial mapping is nonlinguistic, it may well underlie the generativity of language itself.  “In the rat these elements may be restricted to simple aspects like sounds or smells, and we may perhaps allow ourselves the luxury of believing our own experiences to be incomparably richer.  Yet the generative component itself probably has a long evolutionary history.  As Darwin famously put it:  ‘The difference in mind between man the the higher animals, great as it is, certainly is one of degree, and not of kind.’”

© 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.