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- Heikki Tanila.
- Duodecim. 2015 Jan 1; 131 (3): 243-8.
AbstractFor more than a quarter century, the research of and drug development for Alzheimer's diseases have been governed by the amyloid plaque hypothesis, whereby deranged metabolism of the amyloid precursor protein leads to the formation of extracellular amyloid plaques, which in turn causes the activation of microglial cells, destruction of neurons and a progressive memory disease. The ending of three extensive clinical trials in disappointment has raised the question whether the amyloid plaque hypothesis is the correct starting point in the development of curative treatment for Alzheimer's disease at all. Two commencing new trials with patients that are still symptomless will be the final challenge for the hypothesis.
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