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.
so as long as the APO A1 by the way which can bind to an LDL receptor or the scavenger receptor same with the AP OE the neuron can grab them and either internalize them or delipidated particles can go right back and fill up at the asite again
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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.
and once it joins the bloodb brain barrier what is the small APO A1 looking for an HDL buoyancy particle so it joins with the apoe particles so the brain lipoproteins are all apoe or they're all apoe plus apoa1 and you can have multiple copies of each of those on those particles