The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
we find that enzymes like phospholipase a2 are upregulated and activated in the apoe4 brain to perhaps extract fatty acids from its own myelin sheath to produce atp and that tells us about that recommendations that we should give the younger apoe4 carrier may be completely different than a recommendation that we give an older apoe4 carrier who is in a state of energy deprivation and energy failure
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
we found out that a specific enzyme known as phospholipase a2 which is the calcium dependent version of phospholipase a2 is strongly upregulated in alzheimer's disease brains who carry the apoe4 genotype compared to non-alzheimer's disease brains who carry the apoe4 genotype so we had access to a large database of brain tissues from rush rush has one of the largest alzheimer disease research centers in the country and we looked at many enzymes and stumbled across cpla2 and showed that cpla2 is hyperactivated or phosphorylated in e4 ad brains