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The claim for Plexin-b1 seems to be in the area of a reduction in Amyloid plaque...and there is still questions about Amyloid plaque being an effective gateway... to a reduction in Alzheimers activity.

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As I outlined in the below link I think they have it ass backwards when it comes to amyloid plaques. Amyloid plaques look to be another symptom of the underlying cause of the disease. So they may be useful in diagnosing the disease but not in treating it. Both Plexin-b1 and CCR5 increase due to inflammation causing conditions.

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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.
https://investorshangout.com/post/view?id=6693969

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