The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
other genes like clotho uh so there's one variant of clotho klvs which attenuates risk in E4 so an E4 carrier so an E34 carrier that has the cloth okay LVS variant their risk returns to that of a 3-3 a 4-4 carrier who has a cloth okay LVS their risk returns to almost a 3-3 it's still slightly higher um but nowhere near the 4-4 risk
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
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.
if an individual carried KVs the apoe4 or didn't matter so let me break down what that actually meant in their experiment that meant um that in those people that carry apoe4 if they were also heterozy for KVs they had um a decreased risk for developing El Alzheimer's disease that was pretty close to the normal population they had a decreased conversion from MCI to ad and they had decreased um Alzheimer's biomarkers both in their CSF and in their brain they just had less amalo beta
in individuals with um with apoe4 that were carriers of klvs that they just had um less of the effects of AO E4 in terms of less a beta deposition less cognitive problems
he indicated that the 44 also a associated with with the protection from the KBS heterozygosity so that that the effect of having one apoe4 wasn't different than H um having two Apo e4s in terms of KVs protection it protected in both heterozygosity and homozygosity of the APO E4 again it's it's um again just through verbal communication it might have been in a supplement somewhere