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Alzheimer’s
Disease: Prevalence and Cause
Alzheimer's disease prevalence
 Alzheimer's
disease is the most prevalent cause of dementia, accounting for
between 55% 65% of all cases of dementia. While there were fewer than
3 million cases of Alzheimer's disease diagnosed in the United States
in 1980, the Census Bureau predicts there will be more than 10 million
American citizens with Alzheimer's disease by the year 2050. The
prevalence of this disease is believed to double with every five year
period of time between the ages of 65 and 85 years old.
Some researchers
separate Alzheimer's disease into senile and pre-senile forms,
although the two disorders actually represent the same pathological
process. However, the early-onset type (onset before the age of 65)
of Alzheimer's disease is usually associated with a more rapid course
of progression than the later-onset type.
Alzheimer's
disease affects women at a rate of 3 to 1 over men (although the
reasons are unknown). Also, at least one study has suggested dementia,
including Alzheimer's disease, is more common in black then white
American women. Interestingly enough, comparison of population
studies in various countries show distinctly similar prevalence
rates.
Alzheimer's disease cause:
The cause and
pathogenesis of Alzheimer's disease is unknown. It is believed that
multiple causative pathways are likely involved in this disorder.
There have been many hypothesis regarding the cause and progression of
Alzheimer's disease including genetic factors, slow or unconventional
viruses, defective membrane metabolism, endogenous toxins, autoimmune
disorders, and neurotoxicity of such trace elements as aluminum and
mercury.
It is known that
the brains of individuals with Alzheimer's disease contain senile
plaques, neurofibrillary tangles and Hirano’s bodies. There is a
deterioration of nerve cells, but the atrophy seen on neural
diagnostic examination may be more the result shrinkage of neurons and
the loss of dendritic spines then of the actual neuronal loss.
Certain parts of the brain, such as the association cortex demonstrate
the most apparent changes, with early decay in the primary motor and
sensory areas being relatively spared from these changes. Cholinergic
abnormalities are exhibited in the neurochemicals of the brain. There
is a significant decrease in acetylcholine in most individuals along
with decreased immunological activity of somatostatin and
corticotropin-releasing factors. The enzyme required for
acetylcholine synthesis, choline acetyltransferase, is also
significantly reduced. Other studies seem to suggest involvement of
the noradrenergic and serotonergic systems in later-onset Alzheimer's
disease and reduced gamma-aminobutyric acid (GABA). Although it is a
well-known fact that the involvement of cholinergic transmission along
the hippocampus and nucleus basalis essential to the ability to learn
new information, it is believed that many of the symptoms of
Alzheimer's disease are not totally explained on the basis of
cholinergic abnormalities. Investigators continue to examine a
variety of other potential causative or contributing factors.
Researchers have
also investigated the role of beta-amyloid protein in Alzheimer's
disease, and some even believe that this material, a significant
component of all plaques, is a major contributor to the
neurodegenerative changes associated with the disease, possibly both
initiating and promoting the disease process. This assertion is also
supported by genetic studies of families with heritable forms of
presenile dementia, which seem to indicate that disease occurrence is
linked to mutations involving beta-amyloid-related systems. Also,
some investigators have focused on the neurofibrillary tangles and the
identification of a major component of its helical filament, the tau
protein. These researchers have considered the possibility that
modification of tau protein, predominantly by phosphorylation, is an
important feature in the development of Alzheimer's disease.
Some information from DSM-IV-TR
Mental Disorders Diagnosis, Etiology & Treatment
Additional
Information and webpage by
Paul Susic
MA
Licensed Psychologist Ph.D. Candidate
(Health and Geriatric Psychologist)
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