Posts Tagged ‘Buckner R.L. et al’

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.

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