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.