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Posted on 10/28/2011 11:36:30 AM PDT by decimon
For decades the amyloid hypothesis has dominated the research field in Alzheimer’s disease. The theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques, toxic clusters of damaged proteins between cells, which eventually result in neurodegeneration. Scientists at Lund University, Sweden, have now presented a study that turns this premise on its head. The research group’s data offers an opposite hypothesis, suggesting that it is in fact the neurons’ inability to secrete beta-amyloid that is at the heart of pathogenesis in Alzheimer’s disease.
The study, published in the October issue of the Journal of Neuroscience, shows an increase in unwanted intracellular beta-amyloid occurring early on in Alzheimer’s disease. The accumulation of beta-amyloid inside the neuron is here shown to be caused by the loss of normal function to secrete beta-amyloid.
Contrary to the dominant theory, where aggregated extracellular beta-amyloid is considered the main culprit, the study instead demonstrates that reduced secretion of beta-amyloid signals the beginning of the disease.
The damage to the neuron, created by the aggregated toxic beta-amyloid inside the cell, is believed to be a prior step to the formation of plaques, the long-time hallmark biomarker of the disease.
(Excerpt) Read more at lunduniversity.lu.se ...
>>I think it may always have been there, but past generations always died off from smoking and drinking before Alzheimer’s kicked in. <<
Actually, I am not a smoker but I think that the huge boost in Alzheimer’s is due to quitting smoking in that generation.
They are doing research on nicotine reducing Alzheimer’s symptoms.
If doctors would tell patients to take extra Niacin when they quit, I think we would have less Alzheimer’s. Just a thought.
TB
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