InvestorsHub Logo

Cyosol

10/06/22 3:13 PM

#20314 RE: HANUMAN #20313

Clickbait article that completely misses the point.

Here's what the actual paper says:

"In conclusion, higher soluble Aß42 levels are associated with reduced risk of CDR progression, normal cognition, normal hippocampal volume, and normal precuneus metabolism to a greater extent than lower brain amyloid, lower p-tau, and lower t-tau levels in amyloid PiB-PET-positive individuals with autosomal dominant AD-causing genetic mutations. Brain toxicity in AD may be predominantly mediated by a reduction of the soluble protein pool, its functional fraction, rather than its accrual into amyloids."

https://content.iospress.com/articles/journal-of-alzheimers-disease/jad220808

I couldn't find any mention of beta secretase (BACE) which cleaves APP in the wrong place and actually creates the amyloid beta. They did however mention that BACE1 inhibitors worsen symptoms, which has been proven in several failed trials over the years.

In the ibox there's a 2007 paper where Dr. Alkon et al. explain how the process works:

https://pdfhost.io/v/v0ARwmN0V_doi101016jtips200612002.pdf