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runncoach

02/09/17 8:03 AM

#549 RE: blu_1 #548

Good article and I think the study data in April will answer some/many of those questions. Obviously management does not think treatment improvements would be limited to only those with a genetic disposition to early onset alzheimers, otherwise they would have tailored a study to meet that objective. That's one of the main reasons this study is so important.

You're right, given what we know from the few compassionate use patients, there's no way to tell how long the dosage was given for or how long the benefits persisted, etc. Could these random successes not even be attributed to bryostatin? We just don't know yet. We do know significant improvements in mice and we do have anecdotal improvements in small samples. We'll sure know a lot more in 7-10 weeks. JMHO

F1ash

02/09/17 9:40 AM

#552 RE: blu_1 #548

"In a paper to be published next week, Alkon and his colleagues describe the molecular steps by which bryostatin increases the production of two key molecules to stimulate the creation of new synapses. “That’s what you need, something that gets at the underlying disease,” said Alkon. “None of the other experimental therapeutics restores lost synapses and prevents neuronal death.”

"It’s not clear where the “other approaches” that Alkon calls for will come from, given the enduring legacy of the amyloid hypothesis on funding decisions. Alkon, working primarily with Rockefeller funding and industry support, focuses on the core pathology of Alzheimer’s — loss of synapses and death of neurons — and has developed a drug called bryostatin. "


Recognize George Perry's name from anywhere?

"The field has known for over 10 years, probably 15 years, that the models were not Alzheimer’s disease and could not predict therapeutic efficacy,” said neurobiologist George Perry, dean of the College of Sciences at the University of Texas at San Antonio. “The models are, at best, models for amyloid and tau deposition, and even that is questionable. These mice never really develop Alzheimer’s.”
https://www.statnews.com/2016/07/28/alzheimers-drug-failure/


One should always be careful not to extrapolate data from a very small patient pool into a sign of the same effect if a large patient pool. That being said, we will all have a much more reliable data set to analyze very soon (April). BP will be much more likely to give credence to the results if successful because of the blinding and placebo. Here is the test they are evaluating in the current trial.

http://www.medafile.com/zyweb/SIB.htm

seventhwave

02/18/17 2:07 AM

#911 RE: blu_1 #548

This looks and quacks like a high-school experiment. No MMSE, Cogstate, p300, etc. just an "i told you so"
Tiny group genetically predisposed to Alz. (reminds me of the Chilean tribe or was it Colombian) what is it - 0.5% of all Alz patient population?
Antibiotic trial design for Alz trial? 3 weeks?
what's the safety profile?
Ticker symbol (NTRP) shows up in this so called "Journal of Alzheimers Disease) WOW!!!
$100m+ mktcap???