Tobe Chuka Umerah
The Psychology of Aging
March 24, 2021
Time is an inescapable construct of reality, carrying unavoidable effects on biological life. This mantra proves true when examining the human species. Genetic and metabolic processes culminate, imposing detrimental effects upon physical and cognitive capabilities alike. Critical analysis of these processes, and their subsequent consequences, elucidates opportunities for intervention and management. This achievement is of clinical, academic, and societal value, as the effects of age related cognitive decline impose severe costs upon the healthcare system, while exposing family members to an emotionally and physically taxing experience.
Aging imposes drastic effects upon the physical and cognitive capabilities of the human body. Muscles waste away, while bones grow structurally compromised. However, the true strength of the human body does not lie in the femur or bicep, but the mind instead. Unfortunately, aging does not spare the mind as time wages war on the human body. To deconstruct the effects of aging upon the mind, the causes must be thoroughly deconstructed. An array of genetic, metabolic, structural, and iatrogenic factors directly results in the progressive decline of cognitive capabilities. Inspection of these causative factors provides insight into the phenotypical presentation observed in the aging population.
One of the most influential effects of aging lies in the longitudinal genetic changes observed at the molecular level. As well known, cells in the human body are readily replaced in response to trauma, dysfunction, or programmed cell turn over. The replication and replacement is directed by genetic material, such as DNA. DNA is located in the nucleus of the cell, and is coiled into chromosomes. Chromosomes, however, are vulnerable to degradation from internal repair and maintenance systems. Telomeres exist to protect against these processes. However, an end replication problem results in progressive shortening of the telomere caps with each occurrence of cell division. After years of replication, telomeres reach a critical length where DNA cannot adopt a protective secondary structure. Cells are unable to replicate, and existing DNA remains prone to degradation and mutation. The proliferative arrest in cellular replication results in senescence and mitochondrial dysfunction. Underlying genetic dysfunction, resulting from years of progressive replication, or aging, may account for the decline in cognitive functioning observed in the elderly. However, current research remains inconclusive. It is unclear whether telomere shortening induces cellular senescence, or if cellular senescence induces telomere shortening (Zhu, et al., 2019). Additional investigation is required to fully deconstruct the role of telomere length in aging. However, telomeres do not present as the only causative agent inducing detrimental effects during aging. Additional mechanisms have been identified to play a significant role in the decline of cognition in the elderly.
As is all too well known, the body’s metabolism decays with progressive age. Untrained observers readily recognize this physiological change, as weight gain grows common and energy levels wane (Barzilai, et al., 2012). However, a clinical investigation reveals more discrete and wide-ranging changes. Of particular concern, the thyroid gland displays age-related changes. The mechanism of action is unclear. However, whether due to telomere mediated senescence, or underlying autoimmune diseases, the thyroid gland functions less optimally with increasing age. This is concerning for cognitive stability, as the brain maintains strict physiological parameters for thyroid hormone levels. Small fluctuations in thyroid levels negatively impact neuronal metabolism, available energy, and in turn, cognition. Moreover, inadequate thyroid levels have displayed constrictive effects upon neural arterial supply, diminishing oxygenation and function (Begin, et al., 2008). This physiological relationship proves damning for the elderly.
As aforementioned, thyroid function decreases linearly with age. Individuals of sixty-five years of age and older display an increased prevalence of subclinical hypothyroidism, resulting in diminished thyroid hormone levels. Further supporting the role of the thyroid gland in cognition, elderly individuals with reduced thyroid hormone levels display diminished cognitive processing speed and working memory capacity (Begin, et al., 2008). However, sharing similarities with the investigations of telomere shortening, the influence of thyroid dysfunction remains inadequately explored. Further research is necessary to confirm the correlations observed between thyroid levels and cognition in the elderly.
The thyroid imbalances observed in the elderly are one metabolic correlation observed with cognitive decline in the elderly. However, additional metabolic processes may be at play. Normal cellular metabolism within the cerebral cortex can result in senile plaques and neurofibrillary tangles as an unwanted byproduct. In a healthy subject, these plaques and tangles are metabolized and cleared. However, in the aged and metabolically compromised brain, the creation of plaques and neurofibrillary tangles outpaces clearing mechanisms. Excess accumulation of these unwanted byproducts results in disrupted synaptic transmission, and even apoptosis. Once a critical mass is reached, cognitive function becomes observably degraded. This disruption in cognition in the presence of plaques and tangles is clinically categorized as Alzheimer’s disease. The phenotypical effects of aging on cognition are addressed in further detail in the following section. However, Alzheimer’s disease imposes a profound effect upon memory, language, and personality, ultimately resulting in death (Saido, 2013). While metabolic dysfunction possesses clear correlations with cognitive decline, additional elements of aging impose effects upon cognition.
Genetic and metabolic causes of aging-induced declines in cognition have been addressed. However, another statistical likelihood associated with increased age imposes an effect upon cognitive capacity: trauma. Several trauma-related risk factors affecting cognitive integrity increase with progressive age. Vascular insults, such as transient ischemic attacks, or stroke, increase in likelihood exponentially with age. While the physical impairments associated with stroke often take the forefront of concern, severe cognitive consequences arise from such a dramatic vascular insult as well (Coco, Lopez, & Corrao, 2016). However, internally induced catastrophe is not the only traumatic event that increases proportionally with age. Direct trauma increases with age as well. Falls, which increase in prevalence with age, often induce concussive damage on the cerebral cortex, influencing cognitive capacity. The elderly brain is more susceptible to traumatic events, and is less suited to manage their detrimental effects (Salisbury, et al., 2018). However, not all cognitive detriments are the direct consequence of the elderly individuals aging processes and behavioral choices. Iatrogenic effects are capable of negatively influencing cognition in the elderly individual as well.
Individuals aged sixty-five an older encompass just twelve percent of the United States population. However, this demographic accounts for thirty-four percent of all prescription medication use, and roughly thirty percent of all over the counter medication consumption (American Public Health Association, 2005). Unfortunately, the utilization of these medications is poorly managed. Medication interactions and individual side effects are a significant cause of impaired cognition in the elderly. Current research suggests iatrogenic pharmacologic management of non-cognitive conditions results in disrupted cognition in up to thirty percent of cases. Histamine receptor antagonists, cardiac medications, corticosteroids, and antibiotics have all been correlated with acute and chronic confusion and cognitive disruption in the elderly (Moore & O’Keeffe, 1999). Nonetheless, they continue to be prescribed to poorly managed elderly populations, despite potential adverse consequences. Iatrogenic effects, trauma, metabolic dysfunction, and genetic degradation are all significant causes of cognitive decline in the elderly. These negative factors work independently and in unison to produce structural and phenotypical changes readily observable in the elderly population.
Several structural changes are readily observable in the aging brain. The brain is composed of neuronal cell bodies and myelinated axons. The grey matter of the brain is densely populated with cell bodies, while containing few axons. Conversely, the white matter is saturated with axons, while possessing few cell bodies. Structural changes are visible in both of these domains within the aging brain. Grey matter volume begins declining after the age of twenty, with atrophy most prominent in the prefrontal cortex, a region responsible for executive planning and higher order thinking. Paralleling this trend in increasing severity, white matter volume significantly decreases as an exponential function of age (Harada, Love, & Triebel, 2013). The structural changes observed in the neuronal structure of the aging brain are accompanied by phenotypical changes as well.
The causes of age related cognitive changes, and accompanying structural degradations, are of little importance if they are not correlated with phenotypically observable behavior changes. Unfortunately, behavioral changes are readily observable in the aging population. Intelligence is categorized into two categories: crystallized and fluid intelligence. Crystalized intelligence is categorized by skills that are reinforced and practiced throughout life, such as vocabulary and motor tasks. Outside of severe degradation, such as Alzheimer’s disease, the aging process does not traditionally affect crystalized intelligence. Fluid intelligence, however, is dramatically affected. Fluid intelligence encompasses higher order cognitive tasks, such as processing speed, attention, memory, and executive function. These skills decline at a rate of -.02 standard deviations per year after the third decade of life (Harada, Love, & Triebel, 2013). The effect on fluid intelligence is readily observable by peers, family, and medical physicians.
Processing speed presents as one of the most dramatically influenced components of fluid intelligence. Diminished processing speed affects verbal fluency, resulting in the altered lingual skills observed in the elderly. Moreover, processing speed affects motor processing, requiring excess time dedication for seemingly simple motor tasks. Compounding declines in processing speed, the attention span of the aging brain is compromised. Selective and divided attention is degraded in the aging brain. The damages to attention, coupled with processing speed inadequacies, impacts the elderly’s ability to multitask, a readily visible dysfunction. With diminished processing speed and attention capacity, is unsurprising memory is negatively affected in the aging brain. Changes in memory presents as the most common cognitive complaint in the elderly demographic. Declarative and nondeclarative memory is both impacted. Declarative memory encompasses the conscious recollection of facts and events. Degradations to this cognitive category explain the inability to recall what was eaten for lunch, or who is the current President. Nondeclarative memory is also impacted. This classification of memory operates unconsciously, and encompasses memory of motor tasks. While crystalized skills, such as riding a bike, are not often damaged, the ability to maintain an unconscious schedule is. These deficits explain the increased likelihood for an elderly individual to fail to maintain medication adherence. Furthermore, executive functioning is degraded in the elderly brain. Executive function is categorized as functions that promote self-sustainability and socially appropriate behavior. Planning, organizing, and problem solving are all governed by executive functioning processes. However, these processes are initiated in the prefrontal cortex, which undergoes progressive degenerative changes as a function of age. In turn, elderly individuals grow increasingly less capable of making decisions that promote an independent lifestyle, as self care and responsible decision making diminish with age (Harada, Love, & Triebel, 2013). Comprehensively, the phenotypical presentation of aging is readily visible. The elderly population displays diminished cognitive capacity that presents in practically every domain of every-day life. These changes degrade self-sustainability, imposing dramatic costs upon the health care system, while emotionally damaging family units.
Fiscal & Social Effects
Elderly individuals with cognitive decline impose an array of medical and practical complications. The decreased capacities for self care results in an increased likelihood of infection and disease. The fall risks associated with poor motor skills and vestibulocochlear dysfunction dramatically increases the likelihood of hospitalization. Moreover, the necessity for supervision of the elderly in nursing home or at home care settings imposes dramatic costs. Estimates suggest the annual cost per capita for the care of cognitive comprised elderly individuals averages $22,300. Albeit, the researchers aggregating this estimate suggest this was a conservative valuation, with true costs likely much higher (Coughlin & Lui, 1989). Nonetheless, a strictly fiscal evaluation would prove amiss. The effects of long term caregiving on families with a cognitively impaired elder prove extremely emotionally taxing. These individuals often require constant supervision and assistance, chaining loved ones to the approaching departure of their family member (Austom & Lu, 2009). With such dramatic fiscal and emotional consequences, strategies to prevent, mitigate, and reverse the processes inducing age related cognitive decline are of utmost importance.
Unfortunately, limited strategies exist to combat the processes associated with age related cognitive decline. As aforementioned, time is an unavoidable construct, and aging is inevitable. However, some strategies have been devised to promote successful and graceful aging, maximizing cognitive capabilities through late life. Maintaining an active lifestyle and engaging in regular cognitive demanding activities has shown success in preventing cognitive decline to due natural metabolic causes. Likewise, a healthy diet, high in antioxidants, has been postulated to convey neuroprotective properties. Avenues preventing disease processes prove similarly break. Several medications have been presented to attempt to postpone the effects of cognitive disease processes, such as Alzheimer’s disease. However, these pharmacological interventions display limited success. Aging is an unpreventable component of life, and cognitive decline appears similarly inescapable. Common sense strategies, such as a mentally and physically active lifestyle, coupled with a healthy diet, present as the only realistic strategy to protect neurocognitive function (Harada, Love, & Triebel, 2013). In turn, additional clinical research is required to ensure the human mind lasts as long as the physical structure it embodies, providing the increasingly large elderly demographic an enhanced quality, and extended quantity, of life.
Aging is an inevitable and tragic component of life. A myriad of processes culminate, degrading cognitive function, and negatively impacting the quality of life for the individual and their social circle. These changes are structurally visible, dictating a physical pathogenic process. However, despite structural, metabolic, and theoretic identification of underlying processes, limited interventions exist to prevent the consequences of aging. Further research is required to identify effective preventative and restorative strategies, mitigating fiscal burdens on the healthcare system, and emotional burdens on the family unit alike.
American Public Health Association. (2005, March 25). Fact sheet: Prescription medication use by older adults. Retrieved March 28, 2021, from https://www.medscape.com/viewarticle/501879#:~:text=People%20age%2065%20and%20older,%2Dthe%2Dcounter%20medication%20use.
Austrom, M. G., & Lu, Y. (2009). Long term caregiving: helping families of persons with mild cognitive impairment cope. Current Alzheimer Research, 6(4), 392-398.
Barzilai, N., Huffman, D. M., Muzumdar, R. H., & Bartke, A. (2012). The critical role of metabolic pathways in aging. Diabetes, 61(6), 1315-1322.
Begin, M. E., Langlois, M. F., Lorrain, D., & Cunnane, S. C. (2008). Thyroid function and cognition during aging. Current gerontology and geriatrics research, 2008.
Coco, D. L., Lopez, G., & Corrao, S. (2016). Cognitive impairment and stroke in elderly patients. Vascular health and risk management, 12, 105.
Coughlin, T. A., & Liu, K. (1989). Health care costs of older persons with cognitive impairments. The Gerontologist, 29(2), 173-182.
Moore, A. R., & O’Keeffe, S. T. (1999). Drug-induced cognitive impairment in the elderly. Drugs & aging, 15(1), 15-28.
Harada, C. N., Love, M. C. N., & Triebel, K. L. (2013). Normal cognitive aging. Clinics in geriatric medicine, 29(4), 737-752.
Saido, T. C. (2013). Metabolism of amyloid β peptide and pathogenesis of Alzheimer’s disease. Proceedings of the Japan Academy, Series B, 89(7), 321-339.
Salisbury, J. P., Liu, R., Minahan, L. M., Shin, H. Y., Karnati, S. V. P., Duffy, S. E., … & Sahin, N. T. (2018, June). Patient engagement platform for remote monitoring of vestibular rehabilitation with applications in concussion management and elderly fall prevention. In 2018 IEEE International Conference on Healthcare Informatics (ICHI) (pp. 422-423). IEEE.
Zhu, Y., Liu, X., Ding, X., Wang, F., & Geng, X. (2019). Telomere and its role in the aging pathways: telomere shortening, cell senescence and mitochondria dysfunction. Biogerontology, 20(1), 1-16.