Disease-Related Cognitive Decline
Possible Causative Factors
Not all cognitive decline is normal. Damage to the brain from cerebral ischemia, head
trauma, toxins, excess stress hormones, or the development of a degenerative dementia such as
AD can lead to exacerbated cognitive declines not expected in normal aging. Cerebral ischemia
can result from events ranging from injury sustained at birth to strokes. It is caused by oxygen
deprivation to a part of the brain for a prolonged period which leads to tissue injury. Brain
damage is irreversible because brain cells are non-regenerative. Head trauma can cause either
direct damage or delayed damage due to increased intracranial pressure (Stradecki-Cohan, 2017).
Brain cells may also be killed, disrupted, or damaged by environmental toxins. The amount
of damage is dependent on the type of toxin in the body. In adults, the most common toxin that
affects the brain is alcohol. Alcohol is particularly dangerous as it can pass the protective blood
brain barrier. This allows entrance into the central nervous system to act on areas of the brain that
are susceptible to chemical changes. It is a common misconception that alcohol only temporarily
affects the brain, causing no permanent damage. However, alcohol abuse has been proven to cause
the white matter in the cerebellum to atrophy. Alcohol can affect neurotransmitters which are
responsible for sending messages throughout the brain. This reduced rate of message
transmission in the brain may cause behavior change and slowed motor function. Although
impaired judgment, slurred speech, and emotional variability are temporary effects of drinking,
the centers that control these functions may become permanently changed as the result of
alcohol abuse (Velentza et al., 2019).
Chronic and repeated stressors are major triggers for constant inflammation throughout
the body. Although the blood brain barrier normally protects the brain from molecules
circulating throughout the body, stress can decrease the integrity of this barriers, allowing
inflammatory proteins to enter the brain. Since the hippocampus is particularly vulnerable to
these proteins, learning and memory may be significantly impacted. The hormone cortisol is
released when the body is under stress. Prolonged high levels of cortisol have been associated
with shrinking of the hippocampus. There are high rates of depression in individuals with
chronic stress due to the changes in brain chemistry and physical response (Sahakian, Langley, &
Kaser, 2020).
Alzheimer’s Disease
Diagnosis
AD is not a part of the normal aging process. It is an irreversible brain disorder that
develops over a span of several years. It is the most common type of dementia. The pathology
of AD is not fully understood by scientists. Although this pathology is frequently diagnosed in
patients, its presence can only be confirmed by a postmortem autopsy. To be diagnosed with
this disorder, a patient must be screened by a healthcare provider using the criteria listed in the
fifth publication of diagnostic and statistical manual. This publication is updated by the
American Psychiatric Association every few years (American Psychiatric Association, 2013).
According to the American Psychiatric Association, diagnosis of AD first requires
evidence of some degree of impaired mental functioning. This impairment must have developed
gradually and affect one or more areas of the brain. The number of areas affected by the disease
helps to determine the severity of the illness. Memory and learning must show deterioration that
is not related to other neurological, psychological, or medical problems (American Psychiatric
Association, 2013).
Pathology
Although the cause of AD is not yet fully understood, there is a recognizable pattern to
the pathology. Cellular changes in the brain which are associated with AD have been found to
occur as early as ten years before the onset of symptoms. There is a sharp decline in the
availability of neurotransmitters in the brain. The axons and synapses are either damaged or
destroyed. This results in decreased attention span, impaired memory, slowed learning, and a
decline in higher cognitive abilities. Although the cause of the damage cannot be confirmed, it
is suspected that neurotic plaques and neurofibrillary tangles are to blame. Neurotic plaques are
composed of amyloid-beta which is formed from misshapen pieces of amyloid precursor protein
(APP). APP is a fibrous protein typically found in synapses of the neurons. When amyloid-beta
is in its soluble form, it binds to neuronal receptors which erodes the synapses. On the other
hand, the insoluble form clumps and is less toxic (Murman, 2017).
In rare cases, AD can be the result of genetic mutations. Damage to the gene
apolipoprotein E (APOE) which is responsible for lipid transport and injury restoration in the
brain is a possible risk factor. Individuals who have the E4 allele have a greater risk of
developing AD than individuals carrying the normal E3. In contrast, the E2 allele decreases
the risk of developing the disease (Hopperton, 2018).
Both degenerative and genetic mutated AD, begin with damage to the hippocampus
leading to the loss of recent memory and the inability to recognize familiar objects. The cerebral
cortex is also affected impacting the patient’s ability to perform certain cognitive tasks and apply
problem-solving skills. This is often due to the buildup of B-amyloid protein on the outer surface
of the neuron which leads to cell injury or death. The accumulation of this substance also blocks
the synapses of the brain. In addition to protein accumulation around the neuron, protein tau also
begins to fill the inside of the neuron blocking nutrients from nourishing the cell. The brain also
shrinks. However, it is unclear whether this is the result of normal aging or accelerated
deterioration caused by AD. These changes do not always indicate that AD will develop, but
they are considered to be risk factors. Physical injuries and illness such as cardiovascular disease,
head injury, or traumatic brain injury may correlate to the development of AD, but this theory
has not been definitively confirmed (Gao et al., 2021).
Symptoms
The presentation of AD depends on the severity of the disorder. Mild forms present with
decreased energy, drive, initiative, and ability to learn. Moderate AD is often presents with
frustration, confusion, and unexpected actions. Patients may forget personal information, dress
inappropriately, experience trouble sleeping, wander aimlessly, and become suspicious of others.
As the disease progresses, the patient forgets familiar objects or faces and needs repeated
direction. This lack of memory can lead to regressive behaviors. Patients may use confabulation
or stories to preserve their dignity. They may have agraphia, aphasia, apraxia, or agnosia.
Alzheimer’s patients tend to put objects in their mouth (hyperorality), requiring constant
monitoring. They may also display hyper-metamorphosis by repeatedly tracing walls. These
behaviors intensify later in the day in a process called “sundowning.” These behaviors cause
those suffering with AD to be misunderstood. Because some of these actions are considered rude
and inappropriate, the typical response is to attempt to change the behavior using punishment.
However, the brain no longer processes reward and punishment properly since the limbic system
is also affected by AD. Often, others perceive the individual to be “gone” or lost to the disease,
making the individual non-relational and a waste of time (Lanctot, 2017).
Treatment
There are currently a few medications available to treat AD. The most common drugs are
cholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists.
Cholinesterase inhibitors prevent the breakdown of acetylcholine, temporarily decreasing AD
symptoms. NMDA receptor antagonists work by regulating glutamate which is vital for
information processing, storage, and retrieval. They also prevent excessive stimulation of
neurons. These medications can be effective for a short period of time if taken consistently.
However, if doses are forgotten the disease can regress to the same severity as though the
medication was never taken to begin with (Halter, 2018).
Covid-19 Pandemic
Definition
The coronavirus pandemic began in 2019 with the spread of severe acute respiratory
syndrome coronavirus 2 (SARS-CoV-2) that originated in Wuhan, China. Attempts to contain
and stop the virus failed, leading to a global pandemic. On January 30, 2020, the World Health
Organization (WHO) declared an international public health emergency and followed up by
officially proclaiming the situation to be a pandemic on March 11, 2020. Covid-19 has quickly
risen to become one of the deadliest viruses in history, amassing over 541 million cases and 6.32
million deaths (Wiersinga et al., 2019).
Effects of Fear
Since the virus was very deadly, multiple precautions were put in place to prevent its spread.
These safeguards included social distancing by six feet, wearing masks and other personal protective
equipment (PPE), and staying at home to avoid contact with others whenever possible. Following
these requirements created an environment of isolation. Daily routines and lifestyles changed
drastically. Curfews were implemented. Businesses were shut down if they were deemed
nonessential. Traditional gatherings of families and friends were either prohibited or individuals
were too frightened to attend. Individuals around the world were subjected to mandatory or
voluntary isolation. This instigated fear of any form of physical contact as individuals became
terrified that they would contract the virus and die (Adolphs, 2013).
Fear is first experienced in the mind and then triggers a physical response. Once fear is
recognized, the amygdala alerts the nervous system. Stress hormones such as cortisol and
adrenaline are released into the blood stream which leads to rapid breathing, accelerated heart
rate, and increased blood pressure. Blood flow to the extremities is increased to prepare the body
to fight or run. The cerebral cortex becomes impaired, leading to poor decision making and poor
judgment. If fear is not alleviated, the hypothalamic pituitary adrenal axis (HPAA) remains
stimulated which results in the prolonged circulation of stress hormones. These hormones put
certain parts of the body on high alert while shutting others down to compensate. This causes a
decline in immunity, inflammation, and digestion. During the pandemic, immunity was repressed
due to fear of the virus circulating the globe. Thus, individuals were more susceptible to Covid-
19 and mortality rates were high (Adolphs, 2013).
Resident Experiences
When individuals were sick during the pandemic, there were strict visitation restrictions.
Without physical support hopelessness set in. Patients died alone because family and friends
were not allowed to visit. Even after death, bodies were often inaccessible since they were
deemed to be contaminated by the virus. There was no closure for the living (Abbasi, 2020).
Many people lost their jobs or their businesses due to lack of customers. Children were
sent home from school, so parents struggled to work their jobs and manage childcare and
education. They did not hire sitters for fear of bringing the virus into their homes. Nursing homes
and assisted living facilities were closed to the public to protect the elderly (Abbasi, 2020).
Despite the precautions, many became ill. Although facilities for the elderly were able
to keep Covid-19 out for a while, it soon began circulating through them. Residents would
become very ill and be confined to their rooms. Many failed to thrive in this isolated
environment and developed depression and anxiety. In memory care, it was nearly impossible
to socially distance the residents due to their lack of understanding concerning the situation. A
single caretaker was typically designated to dress in full PPE to care for the needs of the
infected to limit exposure. It is important to note that wearing a mask and face shield impair the
travel of sound. Thus, when working with patients who are typically hard of hearing, it becomes
nearly impossible to communicate effectively. The PPE also interfered with lip reading and
interpretation of facial expressions (Chen et al., 2021).
Family members attempted to remain in contact using FaceTime, phone calls, or window
visits. However, each of these options resulted in frustration due to hearing limitations. It became
necessary to supervise window visits after they were repeatedly found open, defeating the purpose of
the barrier. The only interaction that residents had with other human beings was the caregiver
covered in PPE who entered the room for a few minutes every two hours unless there was a need for
additional assistance. As the pandemic progressed, fear and frustration increased.
In individuals suffering with AD and dementia, these conditions were intensified. They were
particularly difficult to quarantine because they did not understand why they could not leave
their rooms. Often, they refused medications out of confusion which caused increased
suffering (Abbasi, 2020).
Caregiver Experiences
When the pandemic began, healthcare workers were reluctant to continue working and
risk bringing the virus home to their families. New rules and regulations placed on staff made
their jobs more difficult. This already understaffed field lost many employees resulting in long
hours of overtime for those who remained. The staff were overworked and underpaid. Much
needed supplies became unavailable. Sometimes masks were utilized for weeks rather than one
day as intended to ensure they did not run out. This placed the staff at an increased risk of
catching the virus. Healthcare workers developed headaches from the smell of the mask and
from the straps pulling on their ears for hours on end. Wearing an N95 mask, face shield, hair
net, gown, gloves, and booties, caused them to become overheated. The already hot rooms made
this condition worse. It is difficult to undergo this level of discomfort for extended periods of
time. Therefore, caregivers focus on completing tasks quickly and moving on to the next
assignment. This created a very goal-oriented mindset rather than a caring attitude. Because the
staff were overwhelmed, there was never enough time to call and update families concerning
their relatives (Chen et al., 2021).
References
Abbasi J. (2020). Social isolation – the other covid-19 threat in nursing homes. JAMA,
324(7), 619-620. doi:10.1001/jama.2020.13484
Adisa Olumide. (2019). Why are some older persons economically vulnerable and others not?
The role of socio-demographic factors and economic resources in the nigerian context.
Aging International, 44(1), 202–222. https://doi.org/10.1007/s12126-019-09348-8
Adolphs R. (2013). The biology of fear. Current Biology, 23(2), 79–R93.
https://doi.org/10.1016/j.cub.2012.11.055
Aiken, L. H. (2021). Hospital nurse staffing and patient outcomes in chile – author's reply.
The Lancet Global Health, 9(11), e1502-e1502. https://doi.org/10.1016/S2214-
109X(21)00390-9
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders
(5th ed.). American Psychiatric Publishing.
American Senior Housing Association. (2021, August 10). Understanding the difference between
assisted living and nursing home. https://www.whereyoulivematters.org/assisted-living-
vs-nursinghome/
Cacioppo, J. T., Cacioppo, S., Capitanio, J. P., & Cole, S. W. (2017). The neuroendocrinology of
social isolation. Annual Review of Psychology, 66(1), 733–767.
https://doi.org/10.1146/annurev-psych-010814-015240
Centers for Disease Control and Prevention. (2022, February 22). Interim infection prevention
and control recommendations to prevent SARS-CoV-2 spread in nursing homes & long-
term care facilities. https://www.cdc.gov/coronavirus/2019-ncov/hcp/long-term-care.html
Chatterjee, S. (2022). COVID -19: Tackling global pandemics through scientific and
social tools. Academic Press.
Chen F, Zang Y, Liu Y, Wang X, Lin X. (2021). Dispatched nurses' experience of wearing full
gear personal protective equipment to care for COVID-19 patients in China-A descriptive
qualitative study. Journal of Clinical Nursing, 30(13), 2001-2014. doi:
10.1111/jocn.15753. Epub PMID: 33761152; PMCID: PMC8251170.
Dwivedi, P. & Badge, J. (2021). Maslow theory revisited-covid-19 – lockdown impact on
consumer behavior. Turkish Journal of Computer and Mathematics Education,
12(2), 2445-2450. https://doi.org/10.17762/turcomat.v12i2.2072
Ely, J. (2018). Mere “safe” staffing falls short of therapeutic need. Nursing Standard, 33(3), 23-
23. https://doi.org/10.7748/ns.33.3.23.s14.
Farokhian F, Yang C, Beheshti I, Matsuda H, Wu S. (2017), Age-Related gray and white matter
changes in normal adult brains. Aging Disorders 8(6), 899-909. doi:
10.14336/AD.2017.0502. PMID: 29344423; PMCID: PMC5758357.
Gao, X., Pan, H., Han, Y., Feng, L., Xiong, J., Luo, S., & Li, H. (2021). Quantitative imaging
of amyloid beta peptide (Aβ) in Alzheimer’s brain tissue by laser ablation ICP-MS
using gold nanoparticles as labels. Analytica Chimica Acta, 1148, 238197-238187.
https://doi.org/10.1016/j.aca.2020.12.072.
