Here is what Leqembi does -

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Lecanemab reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events.
https://www.nejm.org/doi/full/10.1056/NEJMoa2212948

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A tip of the hat to someone who posted this study elsewhere.

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CCR5 regulates Aβ1-42-induced learning and memory deficits in mice
https://pubmed.ncbi.nlm.nih.gov/38215963/

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Here is my take on that study -

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They were looking at AB1-42. AB1-42 drives amyloid plaque accumulation and also increases CCR5, CCL3, and CCL4. When CCR5 was blocked it reversed cognitive dysfunction.

For decades amyloid plaques have been touted as a driver of Alzheimer's. As we've seen from the approval of aduhelm, fighting amyloid plaque does very little. Amyloid plaques themselves are almost certainly not the culprit behind cognitive decline. AB1-42 driving increases in CCR5 certainly looks like part of the problem.

One more medical paper added to the thousands of medical papers implicating CCR5 in diseases. Which nobody seems to be paying much attention too.

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