Definition and risk factors for Alzheimer’s disease

Definition of AD

The definition of AD has been mainly construed with respect to its cognitive effects, population it is prevalent in and presumed causes. Armstrong (2009), for instance, observes that AD is “a degenerative disorder of the nervous system affecting approximately 10% of individuals aged 65 or over” (p. 103). Liu, Wang, Zhang, Xia and Chen, L. (2011), basing their definition on the cause, term AD to be a neuronal loss that results from protein dysfunction in the brain. The criteria for diagnosing dementias provided by the American Psychological Association – Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) – support such definitions. According to DSM- IV criteria, any dementia (AD being the most common) must meet particular aspects. Firstly, it must involve a degeneration of memory and at least one of the following (cited in Alzheimer’s Association, 2011, p. 103):

  • impaired coherence in speech or ability to comprehend spoken or written language,
  • impaired ability to identify or recognize objects when an individual’s sensory function is intact,
  • impaired ability to perform motor activities despite motor abilities and sensory function being intact and the individual taken to comprehend the required task and,
  • impaired ability to make sound judgments such as when carrying out complex tasks.

Secondly, such a cognitive degeneration “must be severe enough to interfere with daily life” (Alzheimer’s Association, 2011, p. 209).


AD symptoms are wide-ranging and may differ with affected individuals. However, a common pattern observed in individuals affected by the condition, is that at the onset, there is a gradual increase in difficulty in recalling new information (Alzheimer’s Association, 2011). Such is attributed to “disruption of brain cell function usually begins in regions involved in forming new memories” (Alzheimer’s Association, 2011, p. 209). Other signs that warn of AD include difficulties in planning and solving problems, getting confused of the time or place one is in, impaired judgment, mood and personality changes, curtailed understanding of visual images and withdraw from social and professional engagements (Armstrong 2009; Alzheimer’s Association, 2011). At later stages, AD could impair movement thus increasing ones susceptibility to illnesses such as pneumonia (Alzheimer’s Association, 2011).

AD diagnosis

Physicians make diagnosis of AD following a family history and subsequent assays. The family history, usually provided by a close relative, includes “psychiatric history and history of cognitive and behavioral changes” (Alzheimer’s Association, 2011, p. 2010). Additional assays conducted to confirm the condition include magnetic resonance imaging scans, which identify the changes in the brain, thus rule out any other possible causes of noted cognitive decline (Ukmar, 2008; Alzheimer’s Association, 2011).

Causes of AD

Although the cause of AD is yet to be known, research has postulated that such antecedent may be contributed by multiple factors (Alzheimer’s Association, 2011). One such factor has been suggested to be changes in the brain that lead to “accumulation of the protein beta-amyloid [β-amyloid] outside nerve cells (neurons) in the brain and the accumulation of the protein tau inside neurons” (Alzheimer’s Association, 2011, p. 210). Armstrong (2010) expounding on one of the proteins – the Amyloid Cascade Hypothesis (ACH) – poses that, according to the hypothesis, deposition of the protein leads to senile plaques (SP) and subsequent neurofibrillary tangles (NFTs) result to cell death, and eventually to dementia. In this cascade it is thought that β-amyloid accumulation interferes with communication between neurons leading to their demise (Alzheimer’s Association, 2011). However, in his experiment Armstrong (2011) does not find such a sequence to be probable, noting that SPs and NTFs develop independently and, possibly, are products rather than antecedents of cognitive degeneration that is observed in AD. With respect to the other protein, tau, it has been suggested that “abnormally high levels of tau [inside the neurons] form tangles that block the transport of nutrients and other essential molecules throughout the cell”, eventually leading to cell death (Alzheimer’s Association, 2011, p. 211). Accordingly, such suggested antecedents via protein deposition, argue the cause to be declining neurons thus affecting nervous transmission efficiency.

Despite the lack of clarity on causes of AD, one clear cause has been identified in genetic mutations. Small cases of AD (suggested to be <1%), are noted to involve mutations on various genes: one located on chromosome 21 that encodes the amyloid’s precursor protein, the second, located on chromosome 14 encoding presenilin 1 protein and, the third, located on chromosome 1, anecoding presenilin 2 protein (Alzheimer’s Association, 2011, p. 211). Individuals who inherit such mutations are certain candidates for AD (denoted familial AD), which, in most cases develops before one attains the age of 65, at times occurring at the age of 30 (Alzheimer’s Association, 2011, p. 211).

Risk Factors

Risk factors for AD range from advancement in age, through genetic susceptibility to injuries to the brain. With respect to age, though the elderly are the most susceptible, individuals younger than 65 years without a genetic predisposition could also develop the condition (Alzheimer’s Association, 2011). Genetic risk is heightened for individuals with a family history of AD, while severe injuries to the head could also enhance such risk (Alzheimer’s Association, 2011). Other risk factors include cardiovascular diseases such as hypercholesterolemia in midlife and subtle cognitive impairment that, though not interfering with daily life activities, is evident in ones memory and other cognitive abilities as can be portrayed by cognitive tests (Alzheimer’s Association, 2011). Go to part 3 here.

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