Neurogenetics Effects on Cognition in Aging Brains

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Table of Contents

Aging Brain
Cognitive Changes
Cognitive Deterioration in Aging
Neurogenetics and Dementia
Alzheimer’s Disease
References

Aging Brain

Aging of the body is inevitable over time; it affects all organs, especially the brain. As people get older, the connections between neurons gradually weaken – the brain undergoes significant changes during a lifetime compared to any other part of the body. When a person is born, the brain contains numerous neurons, but the number of connections between them is insignificant. As a person grows older, many neural connections are formed, and they begin to weaken with age.

Alterations in gene expression are the processes by which genetic information from a gene, the so-called DNA nucleotide sequence, is converted to RNA or protein and may play a role in neuronal aging (Grimm & Eckert, 2017). Synaptic plasticity is the primary mechanism by which the phenomenon of memory and learning is realized (Grimm & Eckert, 2017). The genes involved in this process are less active in older people’s brains than in younger people’s minds. They might have more signs of DNA damage that build up over life and contribute to the brain’s aging process. This process is linked with genes modification; it affects the cognitive abilities changes among older adults, significantly impacting their quality of life, including the possible development of cognitive impairments.

Cognitive Changes

Many seniors have difficulty remembering names, numbers, new information, and multitasking. It happens because neural connections in brain areas involved in learning and performing more complex tasks weaken, resulting in slower information processing. However, new research shows that the brain can adapt to these changes (Grimm & Eckert, 2017). According to Grimm and Eckert (2017), in mature and old age, brain changes are reflected in cognitive processes’ neurodynamic. One of their features is a decrease in reaction speed to external motives (Samaras et al., 2019). It leads to a slowing down of mnestic-intellectual operations, which manifests in an increase in the time spent performing work that requires intellectual exertion compared with persons of young and middle age. Another feature of neurodynamic disorders is a reduction in the ability to concentrate for a long time (Samaras et al., 2019). Therefore, older adults get tired faster and are more often distracted when performing work that requires mental stress.

Moreover, it becomes more difficult for older people than for young and middle-aged people to acquire new knowledge and skills while aging. They also find it challenging to work with multiple sources of information simultaneously. The latter may be associated with a decrease in the ability to switch attention and a certain intellectual rigidity (Samaras et al., 2019). At the same time, in a significant number of cases, age-related changes in cognitive functions do not affect memory for current and distant life events. These changes also do not impact skills acquired in the past, vocabulary, the ability to generalize and make inferences, and general knowledge.

Cognitive Deterioration in Aging

Following the modern classification, mild, moderate, and severe cognitive impairments are distinguished. The mild ones represent a decrease in cognitive abilities compared to the individual’s premorbid level, which formally remains within the average statistical norm or deviates slightly from it (Clouston et al., 2020). It is usually reflected in the patient’s complaints and does not cause difficulties in everyday life. A decrease in cognitive abilities characterizes moderate deteriorations, clearly outside the age norm (Clouston et al., 2020). It is indicated in the individual’s complaints and attracts others’ attention, but does not lead to significant everyday life difficulties. However, it can interfere with the most complex intellectual activity (Clouston et al., 2020). Severe ones are a reduction in cognitive abilities, which lead to significant difficulties in everyday life and partial or complete loss of independence.

The onset of cognitive impairment accompanies aging; the ability to learn decreases and people of the elderly and senile age accomplish new information worse. According to Clouston et al. (2020), cognitive decline is noted after 50, but nature and degree vary in terms of the type of study being conducted and its scales. Elderly and senile persons are a heterogeneous group; with increasing age, these groups’ differences in neuropsychological tests’ performance become more significant. Clouston et al. (2020) noted that age-related memory loss occurs in almost 40% of people over 65. Disorders progress within a year to the degree of dementia in 1% of them, and within one to five years in 12–42% (Clouston et al., 2020). The pathogenetic basis of these changes remains insufficiently clear.

Neurogenetics and Dementia

In recent years, a debate has been revived among scientists about what constitutes the process of aging and death. Bae et al. (2018) have found that the brain ages due to the accumulation of mutations in cells. The number of modifications in healthy people’s brains increases smoothly with age, and the rate of their collection differed markedly for the hippocampus and cortex. In general, new mutations appeared in the hippocampus cells much faster than in the cortex’s neurons, explaining why people in old age are worse at remembering information (Bae et al., 2018). According to Bae et al. (2018), age-related mutations appeared in neurons due to two interrelated disorders: errors in repairing breaks in DNA and damage to its strand when oxidant molecules appeared in the cell nucleus. Bae et al. (2018) claim that the brain ages not according to some single program embedded in all cells, but due to the accumulation of random mutations in the genomes. Accordingly, combating oxidants and DNA breaks can slow down memory fading and overall brain aging.

There is another piece of evidence that explores the correlation between brain aging and genetics. Rhinn and Abeliovich (2017) discovered one of the potential aging genes by comparing DNA samples from nearly 2,000 pieces of brain donated to science by people who died of natural causes and did not have Alzheimer’s disease, sclerosis, or other neurodegenerative disorders. By comparing the pattern of gene activity, Rhinn and Abeliovich (2017) identified several DNA regions that influenced the rate of brain aging. This process was most strongly influenced by the TMEM106B gene, a DNA segment responsible for forming connections between nerve cells (Rhinn & Abeliovich, 2017). Another gene called GRN performs similar functions but affects the brain’s aging to a much lesser extent (Rhinn & Abeliovich, 2017). Scientists believe that several dozen more of these genes may be present in human DNA, which controls various aging organs. Studying them will help understand whether it is possible to slow down the aging process and if so, do it.

Alzheimer’s Disease

The genetics of Alzheimer’s disease, the most common cause of dementia, has been studied most thoroughly. This disease’s predisposition can be inherited in both ways: monogenic – through a single mutated gene, or polygenic, which is a complex combination of variants. According to Wong et al. (2020), Alzheimer’s disease is usually associated with a mutation in three genes: the amyloid precursor protein (APP) gene and two presenilin genes (PSEN-1 and PSEN-2). The most common is the presenilin-1 gene mutation on chromosome 14; symptoms, in this case, appear as early as the age of 30 (Wong et al., 2020). The second most common mutation is in the APP gene on chromosome 21 (Wong et al., 2020). This mutation directly affects beta-amyloid production, a protein that scientists believe is the main factor in developing Alzheimer’s disease.

There are multiple variants of genes that, to one degree or another, affect the chances of getting Alzheimer’s disease. Unlike mutated genes of the familial form, all these variants do not severely cause Alzheimer’s disease, but only slightly increase or decrease the risk (van der Lee et al., 2018). According to van der Lee et al. (2018), the best-known and best-studied gene that increases Alzheimer’s risk is called apolipoprotein E (APOE). Factors will depend on their interaction with other genes and factors, such as age, environmental conditions, and lifestyle. The polygenic form usually manifests itself already in the elderly, after 65 years (van der Lee et al., 2018). About one in two patients with Down syndrome who live to be 60 will develop Alzheimer’s disease (van der Lee et al., 2018). The risk is increased because most patients have an extra copy of chromosome 21, which means an extra copy of the gene for the amyloid precursor protein found on this chromosome (van der Lee et al., 2018). This gene has been linked to the risk of developing Alzheimer’s disease.

Thus, many pieces of research show that damage contributes to age-related memory decline and cognitive decline. People with mild mental deterioration and Alzheimer’s disease show more signs of DNA damage than healthy people. Moreover, the brain’s energy needs can make the organ more vulnerable than other tissues to the metabolic changes that occur with aging. Genes, being fragments of DNA, can play a significant role in the development of dementia. In most cases, genes’ effect is indirect; the disease is determined through a complex combination of inherited factors, environmental conditions, and lifestyle.

References

Bae, T., Tomasini, L., Mariani, J., Zhou, B., Roychowdhury, T., Franjic, D., & Riley-Gillis, B. (2018). Different mutational rates and mechanisms in human cells at pregastrulation and neurogenesis. Science, 359(6375), 550-555. Web.

Clouston, S. A., Smith, D. M., Mukherjee, S., Zhang, Y., Hou, W., Link, B. G., & Richards, M. (2020). Education and cognitive decline: An integrative analysis of global longitudinal studies of cognitive aging. The Journals of Gerontology: Series B, 75(7), e151-e160. Web.

Grimm, A., & Eckert, A. (2017). Brain aging and neurodegeneration: From a mitochondrial point of view. Journal of Neurochemistry, 143(4), 418-431. Web.

Rhinn, H., & Abeliovich, A. (2017). Differential aging analysis in human cerebral cortex identifies variants in TMEM106B and GRN that regulate aging phenotypes. Cell Systems, 4(4), 404-415. Web.

Samaras, K., Makkar, S. R., Crawford, J. D., Kochan, N. A., Slavin, M. J., Wen, W., & Sachdev, P. S. (2019). Effects of statins on memory, cognition, and brain volume in the elderly. Journal of the American College of Cardiology, 74(21), 2554-2568. Web.

van der Lee, S. J., Wolters, F. J., Ikram, M. K., Hofman, A., Ikram, M. A., Amin, N., & van Duijn, C. M. (2018). The effect of APOE and other common genetic variants on the onset of Alzheimer’s disease and dementia: a community-based cohort study. The Lancet Neurology, 17(5), 434-444. Web.

Wong, T. H., Seelaar, H., Melhem, S., Rozemuller, A. J., & van Swieten, J. C. (2020). Genetic screening in early-onset Alzheimer’s disease identified three novel presenilin mutations. Neurobiology of Aging, 86, 201.e9-201.e14. Web.

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