A Cure For Alzheimer’s

Another novel cure for this mysterious brain degeneration has stemmed up from a theory put forth by Joe Rogers of Sun Health Research Institute, Arizona, and Pat McGeer of the University of British Columbia, Vancouver. The duo emphatically advocate the use of anti-inflammatory drugs related to common aspirin for treating dementia associated with AD. Rogers and Geer believe that AD is essentially an inflammatory condition very much akin to rheumatoid arthritis—an excruciating disease where a severe inflammation of the joint occurs. “The neurological damage is caused by a locally overreacting immune system in which biochemical and cellular defence mechanisms turn against the brain cells they are mental to defend,” say the researchers. What’s more, the clinical trials with an anti-inflammatory drug named Indomethacin have been quite promising.

Rogers and Geer suggest the involvement of beta-amyloid in the involvement of beta-amyloid in the ‘complement cascade’. Complement cascade is a chain of molecular events producing special proteins which can be fatal to foreign cells. It is triggered when the defense machinery of the body produces protective protein molecules called antibodies to counter the attack of foreign proteins known as antigens. Rogers and Geer seem to be on the right track since various other studies have revealed that amyloid indeed has a ‘short-circulating’ effect. That is, it stimulates this cascade without any antibodies. This eventually causes the slaugher of otherwise healthy brain cells.

Scientists have further discovered that the brain lesions found in Alzheimer’s patients are filled with a special type of cells called microglial cells. These cells in a normal brain function like ‘house-keepers’, disposing dead or wounded nerve cells. But they play a totally different role in Alzheimer’s victims. Not only are they unusually ferocious in devouring the nerve cells but also appear to be secreting toxic protein molecules which belong to the complement cascade.

Running amock, these cells do not even spare the innocent bystanders. To confirm their finding that AD occurs due to an overenthusiastic defense response against the nerve cells triggered by beta-amyloid, researchers have surveyed the hospital records of about 12,000 patients in USA and Canada who suffered from AD or rheumatoid arthritis. Only a small number of these had both the diseases, suggesting a link between susceptibility to arthritis and resistance to AD. This is so because most patients of arthritis take a lot of anti-inflammatory drugs and hence develop resistance to AD.

In yet another exciting study, Mc Geer along with a group of Japanese scientists has shown that the rate of development of dementia is very low in people suffering from ‘leprosy’ –a bacterial disease that specifically affects the nerve cells. This was particularly seen in patients taking ‘dapsone’, the drug of choice used to treat leprosy and a well known antibiotic having a powerful anti-inflammatory effect. The incidence of dementia was found to be as low as 2.9 per cent in patients taking Dapsone compared to 6.25 per cent in those who did not take the drug. Interestingly, the senile lesions that appear in Alzheimer’s patients were found to be conspicuously lacking in the leper brains.

A new avenue of research on AD is wide open. Search is on for better anti-inflammatory drugs which can penetrate the blood-brain barrier and cool the immunological fire, without having any side effects. Drugs capable of blocking the production of beta-amyloid are other contenders for providing relief to victims of AD. Meanwhile, in a breathtaking finding, a team of scientists from Duke University led by Allen Roses could lay its hands on the very segment of the life’s ‘blueprint’ that ultimately decides the fate of the brain cells of a person.

They have shown that two versions of a gene called Apo-E2 and Apo-E3 protect people from developing Ad but another form of the same gene, namely, Apo-E4 almost always causes the disease in its carriers by the age of 80. This spectacular development thus opened the way for designing drugs which could effectively block the activity of the ‘bad’ gene, thus making the impossible possible! This is a glimmering light in otherwise a dark alley of AD.

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