Ann: Prana's PBT2 Directly Restores Neurons C, page-38

re: Ann: Prana's PBT2 Directly Restores N... Stocky, RNAi, there has been some work done there to silence the APP gene which would prevent the production of amyloid. I cant see that would be a good thing now we know amyloid is part of the brains immune system. They have seen some positive mouse results, as have all the drugs which failed in humans. There are many targets
I guess the APOE4 gene, which pre disposes 60% of Alzheimers sufferers to Alzheimers would have to be a target along with the presenilin genes. Problems can arise from selectively targeting these processes because some have multiple uses which are not fully understood. APOE4 is also used in colesterol and triglyceride transport and is needed in normal metabolism.
So there is work ongoing but the risk/benefit is still not clear because all the uses of the genes are still not fully understood. SecretaseB has been identified as a target as mice with no SecretaseB have shown no deficits.

Where these type of treatments fall way short of the mark in my opinion is they all try to take one interdependent part of a very complex system, knock it out, and just hope nothing else will be effected. Lilley knocked out both secretases and ended up with accelerated permanent memory loss and increased skin cancer risk.

PBT2, on the other hand just clears away the trash that is damaging the neurons through toxicity, allowing the brains own iron clearance mechanism APP(Which one RNAi drug has silenced) to normalize iron levels, which had been damaging neurons through oxidation. PBT2 works by taking away the plaques that have been soaking things(critical metals) up, and locking up another of the brains repair mechanisms (amyloid). PBT2 then returns the zinc and copper trapped in the amyloid plaques back to the neurons, where zinc is required for many functions.
PBT2 is attacking the problem on many fronts and the resulting normalization of the conditions around the neurons and synapses, and the normalization of the critical metals in the neurons, results in the brains own complex repair mechanisms being able to do their job.
The above paragraph makes a lot of assumptions, which would be very suspect if it wasnt for the fact they have already reversed cognition loss in a human clinical trial, and demonstrated one of the ways that was achieved with recently published research.
In comparison, I suspect the RNAi drugs have limited use in a complex interdependent system like this. It is thought they could delay onset if they could silence the presenilin genes with no other problems.

All just my opinion. Do your own research.