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]
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/
[2] https://www.frontiersin.org/articles/10.3389/fnagi.2018.0022...
[3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888851/#emmm20...