3 ms·

> All in all, there is no question that amyloid-beta is a key part of Alzheimer. You are responding to an article that very much puts it into question. You sho

by sampo 7y ago

> All in all, there is no question that amyloid-beta is a key part of Alzheimer. You are responding to an article that very much puts it into question. You should read the article, it's not long. But it'll give some quotes: “The amyloid hypothesis has been one of the most tragic stories [in] disease research,” said neurobiologist Rachael Neve of Massachusetts General Hospital. And Making it worse is that the empirical support for the amyloid hypothesis has always been shaky.

zosima 7y ago
Rachael Neve seems to believe, that APP (amyloid precursor protein) has a pathological role through other means than its degradation to amyloid beta, suggesting instead that it may have receptor-like properties [1]. Mostly, as I understand it, from arguments of structural similarity. It's interesting, but I know of very little solid evidence pointing that way. (And the article I could find was quite old) I think suggestions that amyloid beta is part of cellular defense, and that its "designed" to stick to foreign bodies/pathogens, preventing them from spreading in the brain, is more interesting.[2] Early-onset Alzheimer would then be caused by amyloid beta being released erratically, while many of the late-onset Alzheimer cases might be driven by amyloid beta in addition to some underlying inflammatory process. The amyloid hypothesis, strictly interpreted: that amyloid beta is highly neurotoxic through plaque formation and is the sole cause of neurodegeneration, is also known to be dubious and not explain many observations very well. But that doesn't really challenge that amyloid beta plays a significant part in the pathology. [3] [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1862818/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1862818/ [2] https://www.frontiersin.org/articles/10.3389/fnagi.2018.00224/full https://www.frontiersin.org/articles/10.3389/fnagi.2018.0022... [3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888851/#emmm201606210-blk-0001 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888851/#emmm20...

by sampo 7y ago

zosima 7y ago

Rachael Neve seems to believe, that APP (amyloid precursor protein) has a pathological role through other means than its degradation to amyloid beta, suggesting instead that it may have receptor-like properties [1]. Mostly, as I understand it, from arguments of structural similarity. It's interesting, but I know of very little solid evidence pointing that way. (And the article I could find was quite old) I think suggestions that amyloid beta is part of cellular defense, and that its "designed" to stick to foreign bodies/pathogens, preventing them from spreading in the brain, is more interesting.[2] Early-onset Alzheimer would then be caused by amyloid beta being released erratically, while many of the late-onset Alzheimer cases might be driven by amyloid beta in addition to some underlying inflammatory process. The amyloid hypothesis, strictly interpreted: that amyloid beta is highly neurotoxic through plaque formation and is the sole cause of neurodegeneration, is also known to be dubious and not explain many observations very well. But that doesn't really challenge that amyloid beta plays a significant part in the pathology. [3] [1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1862818/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1862818/ [2] https://www.frontiersin.org/articles/10.3389/fnagi.2018.00224/full https://www.frontiersin.org/articles/10.3389/fnagi.2018.0022... [3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888851/#emmm201606210-blk-0001 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888851/#emmm20...