Great to see confirmational research! There's some fascinating info in there about how the brain naturally compensates for deficits in early stages. Eventually, however, the brain is overwhelmed by the disease in later stages.
A few comments:
- We seem to be further advanced in research in other diseases. We've seen research on a disease (fragile-X?) where the shape of dendrite can be brought back to normal with Bryostatin. That might be one of the cascade portions where Bryostatin has an advantage over this compound.
- I agree that PKC-e biomarker (skin test?) will be key to our success in earlier treatment of AD. If/when our trial proves successful, the PKC-e theory will be viewed as a working model, and then we need to fully develop the skin test for this biomarker.
- This research focuses on early stages of AD, but NTRP has shown that reversal is also possible in late-stage disease.
- "causes of sporadic form still unknown and not yet understood". If PKC-e theory is proven, Alkon/NTRP understand it. I believe Alkon is spot-on with PKC-e theory, but it's just a theory for now.
- They comment that the first detection of neuroinflammation and oxidative stress is in advanced AD. I could be wrong, but just like AB plaques and Tau, I believe these are later-stage SYMPTOMS of AD, not the CAUSE of AD.
- Fascinating discussion of synaptophysin, total synaptic area, and compensation in early stages of AD.
- Overall, I think these guys are onto something in that they are looking heavily at the "compensation" stage of AD. However, they still don't understand the CAUSE of AD (pkc-e deficiency theory). Could be developed into a possible treatment, assuming it's safe and crosses the BBB and can be dosed properly.
- Since they are working in earlier stage AD, unless they can come up with a biomarker to shorten the duration of the trial, their trials will take 2-3 years to complete. IMO, it was good strategy by Dr. Alkon to take late-stage AD patients, as the trials can be of shorter duration.
