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Scientists at the Krembil Brain Institute, part of the University Health Network, have proposed a new mechanistic model (AD2) for Alzheimer’s, looking at it not as a brain disease, but as a chronic autoimmune condition that attacks the brain.

This novel research is published today, in Alzheimer’s & Dementia.

“We don’t think of Alzheimer’s as fundamentally a disease of the brain. We think of it as a disease of the immune system within the brain,” says Dr. Donald Weaver, co-Director of the Krembil Brain Institute and author of the paper.

Alzheimer’s disease, the most common form of dementia, isosorbide side effects hair loss impacts more than 50 million people around the world, with a new person being diagnosed every three seconds. Yet, despite more than 200 clinical trials in the past 30 years, there are no disease modifying therapeutics to prevent, halt or treat Alzheimer’s.

“We need new ways of thinking about this disease, and we need them now,” says Dr. Weaver. “To date, most of the approaches in Alzheimer’s research have been based upon the theory that a protein called beta-amyloid, which is supposedly abnormal in the brain, clumps up. And when it clumps up, it kills brain cells.”

“But we believe beta-amyloid is right where it should be. It acts as an immunopeptide — a messenger within our immune system — so that, if we have head trauma, beta-amyloid repairs it. If a virus or a bacteria comes along, beta-amyloid is there to fight it.”

That’s where the problem occurs, says Dr. Weaver. “Beta-amyloid gets confused and can’t tell the difference between a bacteria and a brain cell and so it inadvertently attacks our own brain cells. This, then, becomes what we call an autoimmune disease. The immune system is actually attacking the host, our brain.”

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