[mobilejdral]

The non-DHA omega-3 EPA are good at preventing perivascular fibrosis and thus a better glymphatic system for the removal of beta-amyloid proteins. EPA also helps produce melatonin which kick off sleep and this whole process.

Natto-serrazime is probably an excellent complement as it is on the other side and is a dissolver. (Noteworthy: Pterostilbene + Glucosamine similar to EPA reduces fibrosis)

The interesting connection is how this is needed when we are older, but not younger. When younger ERa activates more which does this all on its own. This is the connection to why 2/3 of alzheimer's are post-menopausal women and why HRT is important.

Edit: and to tie this to APOE as it is the gene most associated with Alzheimer's. e4/e4 requires more choline so someone with e4/e4 is more likely to be choline deficient. EPA/DHA usually attach to Phosphatidylcholine (PC) when in the blood/brain. PEMT is a gene controlled by ERa to make choline, but from the above less ERa activation and we make less PEMT so less choline and less PC. Choline is the precursor to Acetylcholine (primary neurotransmitter for memory and focus and essential for REM sleep). This is why Choline is known to help with Alzheimer's.

[incrediblylarge]

I did a job for some neuroscientists years ago and we found a very strong correlation between microplastics exposure and elevated acetylcholine in a very young sample. They all thought there should be no effect or the effect should be inverted because of oxidative stress. We never resolved the phenomenon though. From what I understand, Acetylcholine elevation in the lipidome is either neuroprotective or neutral. Is there any reason why microplastics exposure would tend to increase acetylcholine?

[mobilejdral]

Depends on the microplastics, but many act as endocrine disruptors that "mimic" estrogen, tricking the body into over-activating ERa and upregulates the PEMT gene and the higher acetylcholine. It could also be that the microplastics can physically bind to or chemically inhibit acetylcholinesterase and that is the reason for the higher acetylcholine. Depending on the cause this is only a short term good thing, but could be downregulating genes.