Alzheimer Disease Fact Sheet

1. Pathophysiology:

i) Biological Basis and Pathology:

Alzheimer disease is a progressive, degenerative disease which is the leading cause of dementia worldwide in adults (Gauthier et al. 1997). The disease is a chronic disease primarily affecting neurological functioning in the elderly, though it is occasionally diagnosed in earlier age (Crowley 2004). The ten warning signs, or symptoms, of Alzheimer disease according to the Alzheimer Society of Canada are progressive memory loss, difficulty performing regular tasks, language problems, disorientation of time and place, decreased judgment, problems with abstract thinking, misplacing items, changes in behaviour, personality changes, and loss of initiative (2005). In affected patients, the disease is characterized by altered physiology of the brain, mainly in the temporal and hippocampal regions (Gauthier et al.1997). Although patients not suffering from dementia may also exhibit considerable neuronal loss in the cerebral grey matter, Alzheimer disease is distinguished by above-average loss of cortical neurons as well as enlargement of the ventricles. In addition to these factors, the dendrites of the surviving neurons in an Alzheimer disease patient may exhibit restricted branching (Hart and Semple 1990). Cerebral biopsies of Alzheimer disease patients typically reveal the presence of large numbers of neurofibrillary tangles and neuritic plaques, although these features are not unique to the disease (Hart and Semple 1990). Neurofibrillary tangles consist of paired helical neurofilaments mainly comprised of the protein tau (which is associated with microtubules). In Alzheimer disease, the filaments precipitate uncontrollably, thereby displacing neurons and ultimately resulting in neuronal loss (Friedhoff et al. 1998). Neuritic plaques, conversely, are accumulations of damaged nerve filaments consisting of в-amyloid protein cores (Crowley 2005). Both tau proteins and в-amyloid proteins are found in normal brains; however, both are found to be abnormal in the brains of patients with Alzheimer disease. The effects and significance of the presence of the abnormal proteins are unknown, and continue to be extensively researched (AS 2005).

As to be expected in patients suffering brain lesions, many disabilities accompany Alzheimer disease. Generally, there is a rather predictable deterioration path the patient follows. Often, there are no symptoms in the early stages of the disease, while there is complete loss of autonomy for regular daily activities as well as severe speech and motor activity failure in the more advanced stages (Gauthier et al.1997). Physical changes may arise at any stage of the disease, though most tend to be characteristic of the later stages. The most common physical symptoms are disorderly walking, abnormal staring and posture disturbance due to increased muscle tone (Hart and Semple 1990).

ii) Subtypes:

Alzheimer disease is typically categorized by mode of inheritance. Sporadic Alzheimer disease is most common, accounting for the majority of cases. The role of hereditary factors in this type remains unclear. On the other hand, familial Alzheimer disease is inherited in autosomal dominant fashion and accounts for less than 10% of the overall prevalence (AS 2005).

iii) Causes:

Research in several different areas is being conducted in attempt to discover the cause(s) of Alzheimer disease. Although the causes of Alzheimer disease are still unknown, many theories have been formulated to explain its development. These hypotheses are explained in the subsequent risk factors sections.

iv) Genetic Factors:

As indicated above, the role of genetics in Sporadic Alzheimer disease is relatively unclear. However, it is known that Familial Autosomal Dominant Alzheimer disease can be inherited if the disease gene is present (AS 2005). Furthermore, research has proven that about one-third of all cases of Alzheimer disease are acquired through a dominant inheritance pattern (JHU 2005). Therefore, family history certainly plays a role in the

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