Mon Jul 26, 2004 1:29 am   Reply with quote      

A study shows that Hispanic and black Americans are more likely to suffer symptoms of Alzheimer's disease at an earlier age than their white counterparts. I always find a report like this interesting. Despite the fact that number of issues related to racism and discrimination are getting solved(slowly but surely), the disparity is still high. I wonder if Hispanic and black Americans are more prone to Alzheimer's disease genetically or there is something else.

Mon Jul 26, 2004 1:44 am   Reply with quote      

Is it possible that drug abuse, alcohol abuse and smoking, that are higher in Hispanic and Black communities then among Whites, contribute to this disparity?

Mon Jul 26, 2004 1:48 am   Reply with quote      

That's very possible. The article doesn't mention it specifically, but, how should I call this, life style? differences in life style between different ethic and social groups can be the cause.

Mon Jul 26, 2004 1:58 am   Reply with quote      

Discussion on possible causes of Alzheimer's disease has been brought up, so I'd like us to look at Alzheimer's disease's etiology.

Etiology

Three competing hypotheses exist to explain the cause of the disease.

The oldest hypothesis is the "cholinergic hypothesis". It states that Alzheimer's begins as a deficiency in the production of acetylcholine, a vital neurotransmitter. Much early therapeutic research was based on this hypothesis, including restoration of the "cholinergic nuclei". The possibility of cell-replacement therapy was investigated on the basis of this hypothesis. All of the first-generation anti-Alzheimer's medications are based on this hypothesis and work to preserve acetylcholine by interfering with acetylcholinesterases (enzymes that break down acetylcholine). Results had from these medicines have not been promising. In all cases, they have served to only slow the progress of the disease and have neither halted nor reversed it. These results and other research have led to the conclusion that acetylcholine deficiencies may not be causal but are a result of widespread brain tissue damage, damage so widespread that cell-replacement therapies are likely to be impractical.

The other two hypotheses are of generally equal acceptance. "Tau-ists" believe that the tau protein abnormalities come first and lead to a full disease cascade. "bA-ptists" believe that beta amyloid deposits are the causative factor in the disease. For example, the presence of the APP gene on chromosome 21 is believed to explain the high incidence of AD in patients with Down's syndrome (trisomy 21).. The terms "tau-ist" and "ba-ptist" are used (lightheartedly) in scientific publications by Alzheimer's disease researchers. A third protein, alpha syncline, which has already been shown to be important in Parkinson's disease, has recently been proposed as the etiological candidate, giving rise to the "syn-ners". By 2004, several researchers have come to the conclusion that Alzheimer's disease may be a "triple-protein pathology", wherein interactions among all three lesions are what give rise to Alzheimer's disease, rather than any one of the three.

There is compelling evidence that genetic predispositions underlie the development of Alzheimer's disease. However, the most obviously genetic cases are also the rarest. Most cases identified are 'sporadic' with no clear family history. It is probable that environmental factors have to interact with a genetic susceptibility to cause development of disease. Head injury has been consistently shown to be linked to later development of AD in epidemiological studies. In addition, small cranial diameter has been shown to correlate well with early onset of recognizable symptoms. The most commonly accepted explanation for this last feature is that larger brains simply may have more cells that can afford to be lost. Inheritance of a specific variation the ApoE gene (epsilon 4) is regarded as a risk factor for development of disease, but large-scale genetic association studies raise the possibility that even this does not indicate susceptibility so much as how early one is likely to develop Alzheimer's. Intriguing work is currently going on investigating the possibility that the regulatory regions of various Alzheimer's associated genes could be important in sporadic Alzheimer's, especially inflammatory activation of these genes.

Studies have not shown strong link with toxins, vitamins, metals or diet, although rabbits fed a high-cholesterol diet in the presence of copper ions in their water did develop amyloid brain lesions and cognitive deficiencies. Likewise, linkage has been found between zinc or copper and reactive oxidative stress contributing to Alzheimer's pathology, and the amyloid precursor protein has been shown to alter expression in response to metal supplementation and chelation. Therefore, it is hasty and premature to dismiss any and all environmental effects out of hand.

Rare cases are caused by dominant genes that run in families. These cases often have an early age of onsent. Mutations in presenilin-1 or presenilin-2 genes have been documented in some families. Mutations of presenilin 1 (PS1) lead to the most aggressive form of familial AD (FAD). Evidence from rodent studies suggests that the FAD mutation of PS1 results in impaired hippocampal-dependent learning which is correlated with reduced adult neurogenesis in the dentate gyrus. Mutations in the APP gene on chromosome 21 can also cause disease.

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Mon Jul 26, 2004 11:14 am   Reply with quote      

It appears that there is some correlation between drug use and Alzheimer's disease.

Without being prejudice, this is very possible.