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Darkhorseman81 t1_iycgvkq wrote

Reply to comment by Relevant_synapse in Alzheimer’s Drug In Development, Lecanemab, May Benefit Some Patients But Carries Risks of Brain Swelling and Bleeding by Relevant_synapse

Amyloid and tau build up in everyone with age. It's just a side effect of loss of nutrient sensing and epigenetic quality control, leading to a build-up of cholesterol and fatty acids between cells, instead of feeding those cells.

A single gene is responsible MOF.

The Max Planck institute have already worked out what causes Alzheimers and all vasculature dementia.

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Relevant_synapse OP t1_iych9ko wrote

If there is no amyloid link, then please explain the changes in CSF amyloid/tau/p-tau composition in AD patients that predate clinical symptoms by years and are now being used as part of AD diagnostic criteria:

https://www.nature.com/articles/s12276-019-0250-2

Note: CSF beta amyloid decreases as AD disease severity progresses, not increases as your hypothesis seems to suggest.

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Darkhorseman81 t1_iychxsz wrote

That happens to everyone, and is a part of ageing and loss of epigenetic quality control/epigenetic drift.

The reason it happens faster in APOE4 variants is because that gene is linked to superior cholestrol efflux across the blood brain barrier, which is also linked to higher IQ, and cognitive resilience in children in 3rd world countries who suffer starvation, chronic dirahhea, or toxic metal exposures.

They don't lose IQ like most do during hardship, due to superior brain cholesterol metabolism. They are cognitive powerhouses.

They want to treat the amyloid build-up as a prescription model to make money, and have you on drugs the rest of your life, while it is little more than a side effect of the core dysfunction of ageing.

Fixing MOF repairs the blood vessels and nutrient sensing, so fatty acids and cholestrol don't build up between cells. It also repairs cellular waste management and repair, which prevents the build-up of TAU and Amyloid in the first place.

Study the effect of MOF(Myst1/Kat8) on blood vessels, cellular waste management and repair, chromatin structuring, the integrated stress response, and neural metabolic imbalance.

I'm telling you, fix the acetylation patterns of MOF, a single treatment would do it, and the condition is fixed.

Maybe have to do it again once every 30-40 years, if we don't find a way to correct epigenetic drift, but it's a quick fix.

Dementia and Parkinsons are even easier. Dementia is the integrated stress response alone, parkinsons is the ISR + PGC1A gene, which regulates mitochondrial quality control, becoming dysfunctional.

MOF is slightly upstream from all of them. A spectrum of the same condition.

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Sarcastinator t1_iycszoc wrote

Could I get a link to this?

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Darkhorseman81 t1_iydbteu wrote

Type brothers in arms, the brain and its blood vessels, or janus faced MOF, into a search engine. Good starting point.

On a phone atm, so it's annoying to post links, until I get back to the PC.

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