Alzheimer’s disease is the most common cause of senile dementia, accounting for about 70 percent of all cases. Although the symptoms of dementia have been widely (and inaccurately) viewed by the public as a standard part of the aging process for a very long time, Alzheimer’s only gained broad recognition as the primary cause of dementia rather recently—the Alzheimer’s Association was formed in 1980.
The symptoms and signs of senile dementia generally, and Alzheimer’s disease more speciﬁcally, include a decline in memory, learning, attention, and judgment, as well as disorientation and increased difﬁculties in communication. Alzheimer’s disease often makes it more difﬁcult to think of the right word, for example. Behavioral manifestations of Alzheimer’s disease include a decline in personal hygiene, as when a person who has a prior history of fastidiousness stops bathing; inappropriate social behavior; and apparent changes in personality. Wandering and forgetting what one is doing can become serious problems also, as this can create a genuine danger. As the disease progresses, the patient eventually becomes incontinent and incapable of self-care. A common pattern in Alzheimer’s patients involves the worsening of symptoms at night—this is known colloquially among care providers as sun downing. It is important to note, however, that Alzheimer’s disease, like most age-related syndromes, follows a widely variable course in different individuals. It has been estimated, for example, that fewer than 10 percent of patients who show the mild impairment characteristic of the early stages will actually deteriorate further.
The visible symptoms of Alzheimer’s disease, as described above, are almost all symptoms of other psychological problems as well, which until recently made deﬁnitive diagnosis only possible after death, as the changes created by Alzheimer’s disease are directly related to changes that occur in the brain. New, noninvasive brain imaging techniques such as fMRI, CT scans, and PET scans are now on the way to making it easier to see the distinctive brain features of Alzheimer’s. The primary cellular changes associated with Alzheimer’s disease are neuroﬁbrillary tangles and neuritic plaques, along with atrophy, or the simple death of neurons.
A neuroﬁbrillary tangle is an abnormal set of twisted threads of protein found inside nerve cells. Neuroﬁbrillary tangles appear to interfere with nerve cell functioning by impairing the transmission of impulses down the axon to the next neuron. The distribution of neuroﬁbrillary tangles spreads through the brain as the disease progresses, starting with subcortical structures such as the hippocampus but eventually spreading throughout the cortex. Neuritic plaques are hard, spherical deposits outside the cell walls, formed from proteins that would ordinarily be metabolized. The degeneration of the cells around them leaves spaces called vacuoles, which ﬁll with ﬂuid and granular material.
Without an autopsy and a thorough examination of the brain, it is still possible to diagnose the disease. This process involves noting the history of the impairment, documenting cognitive impairments, and conducting a physical exam, a neurological exam, and a psychiatric evaluation. It is very important to obtain the medical history from a family member, rather than just from the patient. The psychological/psychiatric assessment always includes a mental status exam, which consists of questions tapping the patient’s orientation, memory, math ability, direction-following, motor skills, and other general information. Orientation refers to the patient’s sense of location in space and time and is tested by asking such questions as “Where are you right now?” “What day is it?” and “Where were you born?”
The etiology, or cause, of Alzheimer’s disease is still a subject of considerable debate, but several possibilities have been considered. One possibility is that a virus is involved. This hypothesis receives consideration because another disease involving serious physical deterioration of the brain, Creutzfeldt-Jakob disease (the human version of bovine spongiform encephalopathy, widely known as mad cow disease) is known to deﬁnitely involve a virus. No clear evidence of such a virus involved with the onset of Alzheimer’s has been found yet, however.
Another hypothesis that has received considerable media attention despite scant evidence is the possibility that aluminum exposure is responsible. In support of this hypothesis, unusually high levels of aluminum have been found in the brains of some Alzheimer’s patients. Note, however, that most Alzheimer affected brains that have been examined have not followed this pattern. Other research, however, suggests that rates of Alzheimer’s disease may be elevated in people with unusually high levels of aluminum exposure. Contrary to some media claims, the evidence does not indicate that all cooks should get rid of their aluminum pans just yet.
The most promising area of research into the causes of Alzheimer’s disease involves the possibility of a genetic cause. One possible source of the problem is a protein known as apoliprotein E, which occurs in several sub varieties. The kind a particular brain produces is genetically controlled, and those who have the gene for the type called E4 have a much higher risk for Alzheimer’s disease than those who do not have it. The gene is inherited with an autosomal dominant pattern, meaning it is inherited much like brown eye color—if either parent passes along the gene for E4, the child will have that variety. This may explain why Alzheimer’s disease seems to run in families. Another promising piece of genetic evidence comes from research on Down syndrome. Until the last several decades, persons with Down syndrome rarely lived past childhood or early adulthood, but medical advances have made life past 35 much more common. As this has happened, an interesting pattern has emerged: virtually everyone with Down syndrome who lives long enough eventually develops early onset Alzheimer’s disease. Physiologically, this seems to be because people with Down syndrome develop neuroﬁbrillary tangles much earlier than other people do. The fact that most cases of Down syndrome are caused by mutations to the twenty-ﬁrst pair of chromosomes, usually an extra chromosome, or a trisomy, hence the term trisomy 21, suggests an obvious place to look for a genetic cause to Alzheimer’s. Sure enough, people without Down syndrome who develop very early onset Alzheimer’s also seem to have abnormalities to the twenty-ﬁrst chromosome pair.
At present, no cure is known for Alzheimer’s disease. Treatment largely consists of drugs intended to improve blood ﬂow or to increase levels of the various neurotransmitters affected by the abnormal cells and cell atrophy associated with the disease. No drug regimen has so far emerged as the clearly preferred approach, but various drug and nondrug treatments continue to appear (see Gingko Biloba). Treatment also usually involves full-time nursing care in the more advanced stages of the disease.
- Moore, E. A. Encyclopedia of Alzheimer’s Disease. Jefferson, NC: McFarland & Company, 2003.
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