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.
this concept that if we can figure out how that happened if we could somehow promote more apeway1 going into the brain into the CSF the data suggests that that might be a very interesting opportunity to blunt or reduce risk of Alzheimer's
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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.
how do you get Apple A1 in the brain by raising it substantially in circulation because unlike Apple e Apple A1 can get through the blood Bray barrier because it's small enough
we think and we have pre-clinical already some evidence for that but we're doing a trial in humans where we tap CSF to look at Apple A1 that if your Apple A1 concentration goes up at the circulation enough you'll push it into your brain and once it's in the brain it takes over the function of this dysfunctional Apple E4
what is the protein that can help here it's only one protein Apple A1 Apple A1 can take over all these functions of Apple E4
APO A1 can Traverse the blood-brain barrier and therefore if you have a therapy that raises apoa1 you can potentially offset the
APO A1 can Traverse the blood-brain barrier and therefore if you have a therapy that raises apoa1 you can potentially offset the damage of a defective apoe in response to apoe4