Posts Tagged ‘Frontal 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.

Using tDCS to Help Children with Developmental Disabilities and to Foster Creativity in Adults

August 19, 2012

An earlier Healthy Memory Blog Post, “Brain Boosts”, described means of boosting the brain’s performance. One of these was transcranial direct current stimulation (tDCS). The current is very small, from 1 to 2 milliamps. This method is much safer than other types of brain simulation as tDCS does not cause neurons to fire directly. It must make the neurons more excitable. When tDCS is applied over the right parietal lobe of the brain, mathematical ability is boosted. When it is applied to the right anterior temporal lobe, visual perception and memory is boosted.

An experiment examining enhancing mathematical ability was summarized in Scientific American Mind1 . Children with developmental dyscalia, a learning disability that affects math skill, served in the experiment. These children were to associate numbers with arbitrary symbols, such as triangles or cylinders. After practicing this task, they were rapidly presented with pairs of symbols of different visual sizes and they had to choose the physically larger one as quickly as they could. On some trials there was a mismatch between the size of the symbol and the magnitude it represented (for example a huge symbol meaning two was paired with a tiny symbol representing 5. Such mismatches could cause a delay in reaction because the impulse to choose the larger number needed to be overridden. The experimental group received tDCS over the right parietal cortex for 20 minutes at the beginning of each of the six training sessions. The control group did not receive the stimulation. By the fourth session the children in the experimental group became slower for mismatched pairs as compared with the matched pairs. This is the performance that adults show when they respond to real digits. The control group showed no difference between these trials suggesting that they had not internalized the symbols meaning. These superior performance lasted for six months, which suggests that this method might someday benefit those with developmental dyscalia.

In a special box2 inside her article on creativity in Scientific American Mind, Prof. Chrysikou of the University of Kansas reports on how tDCS, transcranial direct simulation can foster creativity. She reports a study published in 2011 by neuroscientist Allan Snyder of the Center for the Mind in Sydney in which Snyder and his colleagues used this technique to affect the ability of individuals to solve arithmetic puzzles involving matchsticks. The initial problems could all be solved with a similar strategy, but the approach would not work with the last two problems. These problems required a novel approach. For half the subjects tDCS was used to depress activity in the left frontal cortex, while exciting the right frontal cortex, whereas for the other half tDCS was used to excite activity in the left frontal cortex and depress activity in the right frontal cortex. The former group solved the last two problems at higher rates than the latter group. So it appears that the right hemisphere enhances creativity, whereas the left hemisphere impedes it.

Prof. Chrysikou also provided data that tDCS could also support the generation of novel ideas. She again used the method of suppressing one groups’ left prefrontal cortex while suppressing a second groups’ right prefrontal cortex. Yet a third group received sham simulation. The task was to think of novel uses of objects presented in pictures. The group receiving left prefrontal suppression thought of significantly more novel uses and did so significantly faster than the other two groups. These results support the notion that blocking the cognitive filter by inhibiting the left prefrontal cortex during idea generation can promote creative thought.

To the best of my knowledge tDCS is a research tool and not yet ready for prime time. If and when tDCS moves to practical applications remains an open question.

1Weaver, J. (2011). A Stimulating Solution for Math Problems. Scientific American Mind, March/April p.12

2Chrysikou, E.G. (2012). Tickling the Brain. Scientific American Mind, July/August, p. 29.