(NaturalNews) Turning 30 years of established Alzheimer's dogma on its head, researchers are now increasingly rejecting the theory that sticky plaques in the brain are responsible for the mental degeneration caused by the disease.
"The plaque is not the main culprit in terms of toxicity," said Alzheimer's doctor and researcher Scott McGinnis of Harvard Medical School and Brigham and Women's Hospital.
In Alzheimer's disease, the most common form of dementia, patients' mental functions steadily deteriorate, including their memories and ability to care for themselves. Researchers have long believed that this degeneration was caused by sticky brain plaques of a protein known as amyloid beta. Now, they are instead blaming free-floating pieces of amyloid beta known as oligomers.
"If you say Alzheimer's, everyone immediately thinks that it's the plaques that actually cause the disease. That couldn't be further from the truth," said Andrew Dillin of the Salk Institute in California and the Howard Hughes Medical Institute. "The data actually suggest these plaques are a form of protection that the body tries to put on. So this is a sign that your brain was trying to do something very useful and helpful to you, and the remnant was the formation of amyloid plaques."
In a recent study, researchers genetically engineered mice that could produce oligomers but could not form plaques. Compared with mice that could produce both, the plaque-free mice did not fare any better.
Similarly, drugs designed to prevent the human brain from forming plaques have consistently failed to deliver any improvement in
Alzheimer's patients, and have not slowed the progress of the disease.
If plaques are actually a bodily defense mechanism as the new theory suggests, such drugs may actually make things worse.
"This [plaque] hypothesis is actually completely wrong, and we need a new way to start looking at this
disease," said Dillin. "This is actually not a viable therapeutic avenue."
Sources for this story include:
http://www.reuters.com/article/idUSTRE64B4N120100512.
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