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Comment by echelon | Hacker News Reader

The disease may have multiple causes. I wouldn't at all be surprised if some other area of health decline gives rise to the disease state. A number of investigators are looking into vascular health, for instance.

Here's an article I posted a while back that implicates liver health and was able to mechanistically induce the disease in rat models:

https://news.ycombinator.com/item?id=29393937

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The book "The End of Alzheimer's" by Bredesen postulates that there are around 36 risk factors for Alzheimer's. It takes many of them in combination to cause the disease.

This is why studies isolating just one factor have failed to find a significant correlation. It's why there will likely never be a pill to cure it.

The book suggests therapy addressing all of the risk factors. Most of those are simply healthy living. Personally, I've been bending my lifestyle to conform to those. Can't hurt.

I recommend to take a look at this interview by the very Bredesen, to a scientist called Dayan Goodenowe, working also on the Alzheimer problem. He has a very interesting book called "Breaking Alzheimer" that postulates that DHA Plasmalogen deficiency is causative for Alzheimer. Very interesting stuff:

https://www.apollohealthco.com/facebook-live-plasmalogens-an...

Thanks for the link! Frankly, it sounds too good to be true. But I'm not qualified to judge this.

I agree Dr. Bredesen's protocol probably can't hurt as it advocates a healthy lifestyle and diet, but there is NO evidence that it can prevent or reverse Alzheimers[1], as he claims. Also, Dr. Bredesen charges $1800+ for the protocol[2] in addition to selling branded supplements.

1 - https://www.ucsf.edu/news/2020/05/417431/pricey-protocol-not... 2 - https://www.healthleadersmedia.com/clinical-care/alzheimers-...

There is evidence, but I agree it is not rigorous and does not rise to the level of proof. I hope it can inspire other researchers to research parts of it more thoroughly.

With respect to Dayan Goodenowe and his Plasmalogen theory, I think the Rush study should be reproduced by other groups. I am no qualified to judge it either, but thinking critically, unless some glaring statistical mistakes were made, or error measuring the levels, or simply that plasmalogen deficiency is a biomarker more than causative (he goes at length as to why he considers it to be the latter), we are talking about natural compounds (Plasmalogen precursors, or IV plasmalogens) that do not require FDA approval, so it should be fairly straightforward to fund, develop and test.

“The clinical implications of this study are obvious. This is the first reported evidence of a metabolic phenotype with the same clinical characteristics as the APOE ε2ε3 genotype. The probability of dementia in participants with either a high PBV or an APOE ε2ε3 genotype was indistinguishable”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6523320/

The same team is now launching a phase II study to test Probucol:

https://pubmed.ncbi.nlm.nih.gov/35190446/

"recent studies suggest that increased plasma concentrations of lipoprotein-Aβ compromise the brain microvasculature, resulting in extravasation and retention of the lipoprotein-Aβ moiety. The latter results in an inflammatory response and neurodegeneration ensues. Probucol, a historic cholesterol-lowering drug, has been shown in murine models to suppress lipoprotein-Aβ secretion, concomitant with maintaining blood-brain-barrier function, suppressing neurovascular inflammation and supporting cognitive function."

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