[evoloution]

To save you guys a lot of time (years of reading an artifact-infested literature), let me give you my 5 cents.

The fact that a misfolded protein can lead to aberrant protein aggregation is known for many years and is certainly true for CJD (a big discovery). It is not the first time that people try to pitch the idea that AD is a prion disease.

Apart from a few very powerful individuals in the field, most scientists believe that the amyloid depositions DO NOT CAUSE the disease, but maybe they are a part of the pathophysiological process (immuno response?). Some facts: -Do you see the depositions in healthy individuals? Yes (but fewer mostly in certain areas of the brain) -Do the levels of the amyloid deposition correlate with the degree of dementia? No concensus -Do amyloid deposition in vitro induce neurodegeneration or abnormal electrophysiology? No -Have all drugs so far with published data of phase III clinical trials based on the amyloid hypothesis failed? Yes (maybe the last one not miserably)

But the problem is that the amyloid cascade hypothesis is at this point the only working hypothesis for AD and people do not want to lose their grant money or positions in pharma and go back to begin from scratch to find what is really causing AD.

Source: I work in AD research.

[qCOVET]

Thank you. Great answer!

I vaguely remember from my academia days that there was another protein of immense interest that led to centrosomal aggregation of proteins - a precusor to Alzhemier and it was called something like - alpha-synuclein. Is that a subset of amyloid family ? or different ?