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.
By Paul Susic Ph.D. Licensed Psychologist