baudrunner's space: Is Alzheimer's a disease or not?
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Tuesday, January 22, 2008

Is Alzheimer's a disease or not?

Peter Whitehouse, M.D, Ph.D., is an expert on brain aging. He has written a book titled “The Myth of Alzheimer’s: What You Aren’t Being Told About Today’s Most Dreaded Disease.” In a nutshell, he states that Alzheimer's is not truly a disease but a symptom of aging. He states rightly that the development and progression of Alzheimer's differs from individual to individual, and that it is therefore not possible to develop a singular treatment to effect a universal cure for the disease. He thinks that investments would be better served by putting them toward prevention and care rather than a cure.

brain scans:1. normal 2. alzheimer patient's
PET scans of a normal brain and a brain with Alzheimer's disease

One is tempted to agree. After all, about half of the world's population will develop Alzheimer-like symptoms once they reach the age of eighty. And this statistic does reflect the fact that a pattern of susceptibility does not appear to manifest across the population. But that could reinforce the argument that Alzheimer's is indeed a disease. Some get it, some don't, and the aged are generally more susceptible.

In fact, researchers from the Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University in Guangzhou, China have developed a method to identify genetic correlations of Alzheimer's disease. Using a technique called denaturing high-performance liquid chromatography (DHPLC) analysis of genetic material from Alzheimer's patients and comparing the results with standard control samples an accuracy of 100% detection was achieved for 300 samples.

It has been known for some time that 100% of people with an extra copy of chromosome 21, or Down's Syndrome, will have developed Alzheimer's by the age of forty. The genetic link can not be dismissed. It has long been thought that mutated template genes found on any or all of chromosomes 11, 15, and 21 and intended for the synthesis of normal linear peptide chains yield the defective peptides which become the Beta Amyloid precursor proteins (the prions) which ultimately form the plaques which prop open the calcium ion channels in the cell walls of the brain's neurons to allow unimpeded invasion of calcium ions into the affected brain cell. Their overabundance compromises the structural integrity of the three dimensional scaffolding of the neuron by attacking the Tau proteins, causing the cell to perform apoptosis, or bursting, and forming the characteristic tangles seen in postmortem histological sections. This is the beginning of Alzheimer's.

Certainly, aging is a factor. We establish patterns of behaviour which affect our lives in a compounding manner the older we grow. If we cease all physical activity, our muscles atrophy, we grow fat, and our heart becomes weak from overwork. Similarly, if we cease brain activity beyond the bare minimum required for survival then we are not maintaining the ability of our brains to efficiently grow new neural networks and enhance the old ones. The brain requires exercise just like the muscle, and just like the muscle it wears down with old age. That process is irreversible, but not so that we cannot forestall the inevitable as best we can with diet and exercise.

The similarity between Alzheimer's and BSE's (Bovine Spongiform Encephalopathies) cannot be overlooked. Humans can catch a variant of BSE called VCJ (Variant Creutzfeld Jacob's) disease by ingesting a sample, usually of the sweetbreads, from an animal infected with BSE. Alzheimer's and VCJ are both prion diseases and the prion is the vector therefore Alzheimer's should be considered a disease from a pathologist's point of view.

Alzheimer's is a disease, and it isn't. What it is is simply too complex a combination of factors to permit anyone to take a stand on either side and defend it to the exclusion of the other. What needs to be answered are the questions of whether the Beta Amyloid precursor protein is the result of a tired protein synthesis mechanism in the afflicted individual as a symptom of aging or whether the predisposition to Alzheimer's is genetically inherited or whether Alzheimer's is contracted like any other disease, by some prion carrying virus or other vector mechanism. It may very well be a combination of all of the above. If so, that might explain how this age-related disease does not affect half of the population.

The fact that this is a lingering debate points to our as yet incomplete knowledge of Alzheimer's disease.

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