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InTheTrenches

05/20/18 9:13 AM

#6274 RE: Wildginger #6273

Great article. Thanks

runncoach

05/20/18 1:04 PM

#6275 RE: Wildginger #6273

Yes that is a good overview. None of us really know why alzheimer's is gaining more prevalence for sure. So many different theories. Our environment is so different than it was 100 years ago but a key factor is we are simply living 15 years longer than we were even 40 or 50 years ago. Maybe pollution or the types of food we eat or being overweight from lack of exercise or metabolism issues from the same, etc could be the cause, but what can't be refuted is that people are living longer.

This leads me to strongly consider that that brain may "give out" just like the heart or kidneys or liver or other organs "give out". Maybe there is a "master switch" as Dr Alkon refers to with PKCe pathways. IF PKCe deficiency leads to the blocking of processes and growth factors that help maintain synaptic elasticity then you have the cause of so many things that go wrong in the brain as we age. IF PKCe is the answer then you don't have to treat a dozen other things and nibble around the edges as others attempt to do. The bryostatin cascade alleviates those other issues.

Based on the article posted, IF you can develop an early diagnostic for alzheimer's such as measure PKCe levels in the skin for deficiencies and then modulate that level with bryostatin or similar compounds, then you potentially have the discovery of the century. I don't know if that's where we are currently, but I also don't know that isn't where we are with this drug. It's certainly a gamble but that's the way I see it. When we see additional data I think we can make more assumptions to the likelihood of success here, but from what we have seen it certainly cause for attention. JMHO

InTheTrenches

05/20/18 2:09 PM

#6276 RE: Wildginger #6273

One statistic from this article that I find interesting, in relation to our trial:

"In 60% to 80% of dementia cases, the cause is Alzheimer’s disease."

This means 20-40% of patients with dementia don't have Alzheimer's disease.

Does anyone know if everyone who are entered into the Bryostatin trials are verified to have Alzheimer's?

The reason I ask this is because I have discussed the non-memantine subgroup data (14 on Bryostatin and 11 in placebo) with another poster here offline, and we believe there were some non-responders in the Bryostatin group of 14 patients, which brought down the overall scores of the Bryostatin group.

Is it possible that some people with dementia, but not Alzheimer's, were/will be entered in our trials?