It is accepted fact that the underlying cause of Alzheimers is long term exposure to oxidative stress (free radicals). That's not my opinion. As time goes on, the accumlated oxidative insults take a toll and build up. This is prime reason for a lot of the negative sequelae associated with aging. It contributes mightily to the aging process overall. I've heard Alzheimers is a protein misfolding disease, haven't heard it is a disease of synpase loss (tho this a result of Alzheimers). The decrease in synapes is the end result of all these other mechanisms. Addressing synapse degradation is attacking Alzheimers from the backend, not upstream. When Dr. Alkon says bryostatin attacks Alzheimers upstream, he's talking about how the drug "supposedly" potentiates the action of alpha secretase to 'clip' APP so it doesn't have a chance to become a-beta. That's talking about preventing amyloid buildup, which we've discovered is not the root cause of the disease or main problem. Bryostatin doesn't stop the disease process, doesn't prevent it, it tries to address some of the effects of the disease. However, Alzheimers is a degenerative disease, so this approach will become exhausted and overwhelmed at some point.
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