UFAs, fatty acid metabolism and AD pathology

[SusanJ]

Small sample, but they looked at the differences of UFAs found in the brains of deceased folks. Definite difference of amounts between areas of brain and progression of AD. Oh, and they did check ApoE status (small sample, though).

Not sure what to make of it, knowing that COX, LOX and CYP450 produce prostaglandins and leukotrienes, which are highly proinflammatory. And PUFAs, and their metabolites (arachidonic acid from linoleic acid and DHA and EPA from linolenic acid) provide competitive inhibition of COX, LOX and CYP450. (This competition is one of the reasons fish oil can be helpful in RA.)

Perhaps this study is just confirming that the brain is in a huge battle against inflammation as AD progresses, but I don't see that we can say more PUFAs would be "better". Would be interested in what others get out of this (warning, the text is definitely heavy on acronyms - get out a pen and paper to keep track).

Association between fatty acid metabolism in the brain and Alzheimer disease neuropathology and cognitive performance: A nontargeted metabolomic study
http://journals.plos.org/plosmedicine/a ... ed.1002266

[Julie G]

Thanks for posting this, Susan. I read a few press releases yesterday. It’s worth noting that this correlates (across the BBB) with Federoff's finding that a deficiency in peripheral lipids precedes a conversion to AD. I agree that we don’t have enough information to make this actionable, but it’s an interesting data point.

To clarify, six unsaturated fatty acids (PUFAs & MUFAs): docosahexaenoic acid, linoleic acid, arachidonic acid, linolenic acid, eicosapentaenoic acid, and oleic acid are involved. I've only quickly skimmed, but I think a deficiency of all was found, with the exception of DHA.

The authors of the study hypothesize on the significance of their finding:

[This] work suggests that dysregulation of UFA's metabolism plays a role in driving AD pathology and that these results provide further evidence for the metabolic basis of AD pathogenesis.

I don't have time to read the paper, but wonder if anyone has been able to determine if/how this differentially affects E4+?

[SusanJ]

Just updated the title to reflect UFAs. Morning caffeine deficit.