[olsen]

What Causes Alzheimer’s?

...Back in the 1980s, when the amyloid-plaque hypothesis was gaining in popularity, results from our group and from others suggesting that the immune system was playing a major role in the disease were not taken seriously. But today, a new crop of investigators is looking at Alzheimer’s pathogenesis with fresh eyes and finding that neuronal stress and the consequent overexpression of proinflammatory proteins are the likely instigators of neuropathological changes, including both plaque and tangle formation. The idea that amyloid plaques are more likely to be a response to the disease, rather than its initiator, is gaining acceptance...

... So when Rosenberg displayed silver-stained sections from the brains of Alzheimer’s patients showing immune-like cells scattered among the plaques, I couldn’t help but wonder why no one had thought to look at the role of inflammation in this disease. His slides clearly showed enlarged, activated microglia and astrocytes lying among the neurons and amyloid plaques...

... we examined the tau protein and the Parkinson’s-associated α-synuclein (responsible for producing Lewy bodies in that disease), both of which were most definitively linked to Alzheimer’s by Virginia Lee and John Trojanowski at the University of Pennsylvania. Tau is a protein that normally stabilizes microtubules, but when it is excessively phosphorylated at multiple sites, it forms the neurofibrillary tangles associated with Alzheimer’s. The normal function of α-synuclein, the precursor protein of Lewy bodies in Parkinson’s, is still unclear...

http://the-scientist.com/2011/08/31/...mer%E2%80%99s/