Alzheimer’s II
I was provoked to write the post immediately below by this shocking article which suggests possible fraud.
I feel the need to comment on this passage
“Yet Aβ still dominates research and drug development. NIH spent about $1.6 billion on projects that mention amyloids in this fiscal year, about half its overall Alzheimer’s funding. Scientists who advance other potential Alzheimer’s causes, such as immune dysfunction or inflammation, complain they have been sidelined by the “amyloid mafia.” “
WTF ? It is not one or the other. Amyloid beta oligomers bind to tole-like pattern receptors on microglia causing them to release inflammatory peptides (including TNF alpa). TNF alpha stimulates the production of amyloid beta. It isn’t amyloid beta *or* inflammation. It’s as if the chicken researchers said that they have been sidelined by the egg mafia. The two aspects of Alzheimer’s are demonstrably linked.
It seems the assertions with no links was not well received. Here are cites
” tole-like pattern”
It’s “toll-like”, not toll-like.
The hypothesis that abeta is a cause of AD and AD-like dementia is increasingly questioned in the literature. There are several prominent alternate hypotheses, including one that describes AD as type 3 diabetes and suggests that plaques and tangles may be a consequence of neuroinflammation rather than a cause as well as tau-centric causal hypotheses.
https://www.frontiersin.org/articles/10.3389/fnins.2018.00025/full?mod=article_inline
https://www.nature.com/articles/d41586-018-05719-4
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7246646/pdf/ijms-21-03165.pdf
I think humility and understanding of the limits one’s knowledge of literature is essential to any kind of deeper understanding of this complex disease.
@prioritarian
Yes, Toll-like. Named after the Drosophila gene first discovered for its role in dorsoventral patterning in the embryo.
And yes, it still is unclear whether the plaques and tangles are the drivers or are protective, with the soluble proteins causing inflammation and dementia.
This sort of progression from establishment of a paradigm, through a paradigm shift to a new paradigm is hardly unusual in science.
“I think humility and understanding of the limits one’s knowledge of literature is essential to any kind of deeper understanding of this complex disease.” D’accord.