ABetaMale

5 ms·

1.
by ABetaMale 3y ago
The connection is probably that ApoE4 carriers clear out amyloid beta deposits less efficiently than ApoE3/2 carriers (see e.g. [1] among many other sources), whereas microbial infection can induce amyloid deposits to form in the first
2.
by ABetaMale 5y ago
That's a natural a priori hypothesis but there's extremely strong evidence that amyloid is causally upstream. For example, mutations in the enzymes or proteins involved in the production of amyloid-β (APP, PSEN1, and PSEN2), which
3.
by ABetaMale 5y ago
The current most plausible perspective is amyloid-β pathology causes tau pathology which causes neurodegeneration. Thus it's not surprising that amyloid-β pathology can exist without neurodegeneration, if there is no tau pathology (or
4.
by ABetaMale 5y ago
Amyloid-targeting drugs have not failed. There are currently three — aducanumab (phase 2 trial successful, one of two phase 3 trials successful), donanemab (successful phase 2 trial), and lecanemab (promising phase 2 trial which technically
5.
by ABetaMale 5y ago
[1] is probably the study you're thinking of. There's also [2] regarding herpesviridae, among others. In short, there are good reasons at this point to believe that amyloid-β's primary function is as antimicrobial peptide, an
6.
by ABetaMale 5y ago
I've spent about the last two months reading the scientific literature on Alzheimer's, and while there is some dissent, the amyloid hypothesis is currently by far the dominant one, and for good reason IMO. The below is adapted fro