Memory and Aging among the Older Adult
Psychologically, memory is a term used to describe the systematic process through which information undergoes encoding, storage and retrieving when need be. Since as far back as science can trace, older adult’s concerns regarding memory loss continue to alleviate especially with the new knowledge that it symptomizes Alzheimer’s disease. On this note, research has fulfilled its intended purpose of filling in the gap between memory loss in a normally aging adult, and that of an Alzheimer’s victim. Effectively, the new knowledge has served as a relief for aging adults, especially those experiencing occasional memory lapses, because this describes a normal aging and not a symptom of Alzheimer’s as most thought. With this regard, this analysis studies the diverse aspects in memory and aging in the older adult with an analysis of the possible factors contributing to memory loss in pursuit of a better understanding of this issue.
To start with, mild cognitive impairment refers to a disorder characterized by escalated memory problems in the victims as compared to normal persons in the same age bracket. Even though the experienced symptoms do not restrict the victims from carrying on with their normal routine, the influence their self-esteem by instilling the fear of old-age illnesses. For instance, the victims may often misplace items, have difficulties in finding certain words during conversations, or even forget appointments. Research patterns indicate a certain transition between mild cognitive impairment in older adults and Alzheimer’s disease (Coon, et. Al, 2010). Although depicted in minimal cases, victims of mild cognitive impairment experience a 24% possibility of progressing to Alzheimer’s disease annually. This further instills distress in aging adults who simply lose their car keys in the shopping center forcing them to run to specialists.
However, age related memory impairment is related with evident declines in certain memory abilities inclusive of cognitive tasks. A comparative study seeking the effects of aging on various memories found that episodic memory undergoes the most impairment during a normal aging process leading to suppression of tasks such as remembrance of newly encoded information. Consequently, memory decline in aging adults affects their daily lives because it weakens their ability to make decisions gradually reaching a phase that requires more time than ordinary to decide upon petty issues such as what to wear. Furthermore, associative learning indicates vulnerability to the impacts of aging in older adults. This concept best describes the Associative Deficit Hypothesis that argues that the gradual inability to create and subsequently retrieve links between units of information portrays an association between aging and memory decline. Specialists speculate that older adults make use of less effective encoding and retrieval techniques as they grow older because of the diminishing capacity to pay attention (Davies & Janosik, 2008). This is showed by older people’s reluctance to engage in self-initiated encoding procedures as a result of their reduced attentional aptitude. Additionally, this has also been gambled to result from memory self-efficiency claiming that as evident, older persons have suppressed confidence in their own memory performance showed by their alleviated delegation of duties to younger people.
Moreover, the ‘Senior Moments’ phenomenon also describes the aspect of memory and aging as seen in older adults. This memory deficit is demonstrated by an individual’s incapability to embark on a task that they were priory executing before an interruption. In most cases, the individual moves on to another task completely forgetting of the one they were working on at least for some time. This portrays the incapability of an aging adult’s brain to re-engage subsequent to an interruption like an ordinary young mind would. By virtue of this, sequential performance in the aging adult plays a vital role in the sustenance of regular memory functioning such following a normal routine like waking up, showering, clothing, making coffee, and driving to work without necessarily skipping a step. The utilization of memory and inhibitory processes to perform daily activities in a fixed order and not skipping any step in the sequence most importantly facilitates healthy aging in older adults. This is because the memory part of their brain is kept at par with the aging constantly ensuring its continued effectiveness to the adult’s undertakings.
The knowledge about memory and disorders thus results more extensively from the study and analysis of cases that encompass memory loss in the aging adult. Also known as amnesia, memory loss results from damages in different parts of the brain such as the hippocampus, thalamus and hypothalamus amongst others. These damages consequently contribute to the diversification of amnesia. However, other neurological disorders such as Parkinson’s disease and Alzheimer’s disease also contribute to distress in cognition and memory. Moreover, hyperthymesia, also referred to as hyperthymesic syndrome, affects the autobiographical memory of aging adults implying that the victims do not show signs of forgetting small details that would not be stored in normal cases. Although this disorder may be considered as leaning more to the advantageous side, it depicts future memory losses perhaps with precedence in years.
Firstly, medications act as causative agents of memory loss not only in aging adults, but in any person. Evidently, most individuals prefer walking into a chemist directly and asking for medication they think best suits their self-diagnosed symptoms. Alternatively, these individuals receive an over the counter medicine prescription, which in most times comes from unprofessional medicine retailers. This prescription of medicine without prior symptomatic tests leads to the introduction of certain medicines that are currently not required by the body. As a result, the medicines idly remain in the body thus triggering diverse hormonal releases into the body. Consequently, these idle hormones affect the brain activity thus resulting to notable memory loss cases. Possible medicines to this disparity include antihistamines, antidepressants, muscle reluctant, tranquilizers, pain killers, anti-anxiety medications and sleeping peels all of which are mostly used by older adults.
Additionally, drug abuse such as excessive use of alcohol and tobacco contributes to memory decline in individuals. Drugs mainly trigger certain chemical changes in the brain thus making it harder for drug users to recall their memories compared to sober persons. More precisely, smoking leads to the consequent deposition on the walls of the lungs due to smoke. As a result, the smoke reduces the surface area for absorption of oxygen into the body thus leading to depreciated amounts of oxygen available to the body. Reduced amount of oxygen in the body directly translates to lower than normal oxygen levels reaching the brain. Consequently, this reduces the brain’s activity thus depreciation in performance of its tasks. Evidently, smokers undergo more difficulty in matching diverse names to their relevant faces as compared to non-smokers due to their reduced ability of storage, as well as retrieval of information from the memory. Most importantly, this is more fatal to older adults because already their brain is not a state that can handle such strain and remain effective.
Furthermore, derivation of sleep stands out as a renowned cause of memory decline in older adults. This is because both quality and quantity of sleep play a vital role in an individual’s relaxation, thus memory respite as well. Sufficient sleep contributes to acceleration of the speed of consolidating information to the long-term memory thus creating a platform that allows for effective retrieval of stored information. Stress and subsequent depreciation also contribute to memory loss since stress significantly affects memory formation for instance, through learning. This is depicted by the suppressed capability to understand certain concepts under pressure. In depth, the brain releases various hormones, as well as neurotransmitters such as catecholamines and glucocorticoids to counter stressful situations. These hormones and neurotransmitters in turn affect the memory’s encoding process that occurs in the hippocampus. A poor encoding process directly reflects to minimal understanding as well as storage of less than expected information in the memory. Similarly, poor storage of information in the memory means poor retrieval thus illustrating considerable loss of memory. Fink (2000) argues that any memory activity such as learning under stressful conditions alternates to decreased memory recall in individuals.
Fink’s experimental research project to prove this fact incorporated fifty healthy female and male participants subdivided in to a stress test group and a test group. During the sub-division, all factors remained constant to ensure equal subdivision that in turn increased the result’s credibility, as well as its reliability. Under continuous monitoring and consistent recording of their reactions, the participants in the test group had their right hands immersed in cold water for up to five minutes. Oppositely, the control group remained relaxed the entire time awaiting the start of the test. After the initial ten minutes, both groups received thirty words from which they had to memorize as many words as the possibly could. After the availed time for the memorizing stage, both groups were tested to see how much each remembered hence the tests name, free recall test. Furthermore, both groups were asked to identify as many words as they could from a blend of these words together with other words on a large board, also referred to as recognition performance. Resultantly, the stress test group illustrated an impairment of memory performance as it only managed to remember forty percent of the words compared to the control group that recalled seventy percent of the words. Evidently, this research project proves the effect of stress on brain activity. In other words, stress experienced during a learning process that involves brain activity causes distractions to the individual’s minds as it diverts their attention from what they are doing thus affecting the memory encoding process. Deriving from this study, a poor encoding process results to poor storage in the memory and subsequently, poor retrieval thus depiction of memory deterioration.
Nutritional deficiency also acts as a causative agent to memory degeneration especially in older adults who require several nutrients and minerals critically to make up for the loss of the body’s nutrients. Certain proteins and fats facilitate unremitting nourishment of the brain. As a result, poor nutrition either with the limitation or absence of such proteins and fats results to seized brain cell nourishment. Consequently, the brainpower decreases and so does its effectiveness thus leading to frequent experiences of memory loss. Lack of coordination in the three processes; encoding, storage and retrieval of information translates to frequent instances memory rapture. Head injuries also contribute to memory losses as they result to severe brain damages. However, a severe hit to the head to the extent that the damage penetrates the skull could lead to either short-term memory loss or long-term memory loss. The intensity of the hit acts as the key determinant of brain damage and subsequently, memory loss. Moreover, such events that lead to head injuries similarly trigger strokes in extreme severity. This knowledge contributes to the specialist’s advice that any aging adult avoid situations that may lead to possible accidents because at that age, their brain is highly delicate. Strokes, in other cases, involve incidences that cause seizure of blood supply to the brain perhaps following to damaged vessels leading to the brain. Especially in accidents, the damage includes hits that cause bursting of blood vessels causing leakage or blockage. Therefore, this causes insufficient blood supply to the brain. In shorter periods, especially when the victims are rushed to the hospital, they only suffer short-term memory losses that fade away after some time. On the other hand, delayed medication may result to extreme deficiency of blood in the brain thus resulting to long-term memory losses. However, a victim of stroke suffers disability to recall most recent events such as what they had for lunch but may recall their childhood events vividly.
Moreover, dementia is a term used to demonstrate the incessant memory loss as well as other aspects of thinking all severe enough to cause interference with the daily functioning of an aging adult. In that, the continuous loss of memory accumulates to the point that the victim no longer coordinates their actions or maintains their daily activities. Although dementia could be caused by such reasons as blood vessel diseases, extreme drug and alcohol abuse amongst other causes leading to brain damage, the most prevalent cause is Alzheimer’s disease. This disease forms the most prevalent for of dementia, especially on the basis that it has no cure. Its known characteristic of unremitting worsening with continued progression makes it a killer disease as it consequently leads to death in the end. Like symptoms of memory loss, symptoms of Alzheimer’s disease illustrate assumptions of increment with age enforced by manifestations of stress in the victims. To illustrate the link between Alzheimer’s disease as a cause of memory loss, certain factors become known. To begin with, In Alzheimer’s early stages, the most regular symptom is a notable difficulty in remembrance of most recent events. Subsequently, after suspecting Alzheimer’s disease and possible brain scan to confirm its presence, symptoms progress to heightened irritability, confusion, mood swings as well as long-term memory loss. Finally, these symptoms trigger feelings of isolation leading the victim to segregate themselves from their family and gradually lack of coordination of bodily activities leads to death of the victim. With this regard, Alzheimer’s disease evidently becomes one of the major causes of memory decline and loss in its severity as illustrated in its symptoms before leading to the death of its victim (Davies & Janosik, 2008).
Nonetheless, the statuses of the thyroid as well as infectious diseases that cause memory damage contribute to loss of memory. Also called hypothyroidism, an underactive thyroid at the outset contributes to production of limited or depreciated amounts of thyroid hormone. Mainly, the thyroid hormone primarily facilitates the regulation of metabolism in the body through increased basal metabolic rates (Sherwood, 2007). In turn, this increase affects the rate of protein synthesis in the body hence contributing positively to the regulation of growth hormones, as well as neuronal maturation. This is most evident in older adults as a result of malfunction triggered by any of the explained causes of memory decline. In addition to the thyroid’s essence in the proper development and differentiation of all body cells, these hormones further aid the regulation of protein fat. Protein fat inhibits the body’s utilization of energetic compounds, as well as the continuous nourishment of the brain cells (White & Estate Project for Artists with AIDS, 2002). With the knowledge that thyronamines function through similar mechanisms to inhibit neuronal activity, understanding its essence as a cause of memory loss eases up. Relevantly, hypothyroidism leads to lower amounts of thyroid hormones thus minimizing the brain cell’s nourishment. In turn, the brain weakens leading to memory loss. On the other hand, increased levels of thyroid hormone lead to excessive hormones in the brain thus resulting to effective damage on the brain cells. This damage as well, leads to loss of memory in due time hence its full manifestation in older age.
Additionally, diseases such as HIV AIDS and syphilis lead to memory loss following to their effective damage on the brain cells. For example, HIV attacks all body cells simultaneously leading to slow but prevalent damage. In the end, the damaged cells perform inefficiently and with brain cells inclusive, the suppressed performance contributes to the realization of fractional memory losses in the initial stages and long-term memory loss in the end. Nevertheless, aging, though not a negative factor, is a factor that influences normal memory loss in individuals. The constant growth plays a key role in memory loss following to the unremitting deterioration in the effective functioning of the brain cells especially if an individual fails to keep the brain in constant operation. However, this type of memory loss is not opposed since it is the natural way of reflecting an individual’s growth to their cell’s function ability (Recker, 2012).
Lastly, yet importantly, memory loss, though not a proponent disease, has no cure at the moment. However, certain medications show significant effectiveness in controlling an individual’s involuntary memory rapture. Most importantly, aging individuals have a certain degree of control towards prevention of memory loss for instance, avoidance of drug abuse and accepting prescription of medicines only by qualified doctors. In general, avoidance of the above-mentioned causes of memory loss considerably reduces the overall exposure to memory loss. Therefore, this analysis presents a clear and in depth study of memory and aging in the older adult, which may be a stepping stone into a longer brain function best dedicated by exceptional and sustained memory.
Coon, D., Mitterer, J. O., Talbot, S., & Vanchella, C. M. (2010). Introduction to psychology:
Gateways to mind and behavior. Belmont, Calif: Wadsworth Cengage Learning.
Davies, J. L., & Janosik, E. H. (2008). Mental health and psychiatric nursing: A caring
approach. Boston: Jones and Bartlett Publishers.
Fink, G. (2000). Memory and its Function in the Older Adult. San Diego: Acad. Press.
Recker, J. (2012). Scientific Research in Information Systems: A Beginner’s Guide. Berlin:
Sherwood, L. (2007). Human physiology: From cells to systems. Australia:
White, E., & Estate Project for Artists with AIDS. (2002). Loss within loss: Artists in the age of
AIDS. Madison, Wis: University of Wisconsin Press.