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Investor2014

11/08/17 8:41 AM

#129502 RE: imho #129498

You are right, exactly what I thought wrt. Aisen.

Investor2014

11/08/17 8:50 AM

#129506 RE: imho #129498

https://www.medpagetoday.com/neurology/alzheimersdisease/61959

Solanezumab drugmaker Eli Lilly reported the top-line results of the highly anticipated EXPEDITION3 trial in a press release last month. There was an 11% slower decline in disease progression for those on the drug, but the difference on the ADAS-Cog14 wasn't significant at 80 weeks (P=0.095).



Compare that performance over 80 weeks to the Anavex sub-group over 109 weeks.

MycroftHolmes

11/08/17 10:54 AM

#129550 RE: imho #129498

Re: Article

In fairness, there was solid science driving this. Post-mortem analyses of Alzheimer’s patients found their brains were riddled with amyloid plaques. People with a strong family history of Alzheimer’s had genetic mutations in the genes that encode for the production of amyloids. And in animal studies, scientists found that if amyloids were inserted into the brains of transgenic mice, they exhibited signs of memory loss. Remove the amyloids and they suddenly got better. This body of research helped launch the Amyloid Cascade Hypothesis of the disease in 1992—which has driven research ever since.




Insert the plaque, the mice get worse, remove the plaque the mice get better. Post hoc ergo propter hoc... Amyloid is the cause.

But how different is the picture when we simply say, "We introduced a source of inflammation/oxidation and the mice got worse. removed the source of inflammation/oxidation and the mice got better.

Equally true. But now one is looking at ALL causes of inflammation/oxidation not just the plaque.

Academia has an echo chamber problem.

Cheers

Mycroft