Originally posted by pivalde
In the Tanzi's dish we could se clearly how PBT2 made the nerves fire more actively. The only explanation is that the mitochondria produced more energy for the nerves to fire. Tanzi has not published anything about mitochondria in his model but I would predict that he will. He already demonstrated beautifully how the nerves used their increased energy.
Remember this from Max Planck and Merz. They observed synapse recovery with PBT2.
"MELBOURNE, AUSTRALIA--(Marketwire - Nov 14, 2011) - Prana Biotechnology (NASDAQ: PRAN) (ASX: PBT) today announced that scientists from Merz Pharmaceuticals GmbH and the Max Planck Institute presented data showing that Prana's PBT2 improves synaptic activity in neurons needed for memory. The scientists presented their data at The Society for Neuroscience meeting in Washington D.C. in a poster titled "Aggregation inhibitors reverse β-amyloid (Aβ
-induced inhibition of long term potentiation (LTP) in murine hippocampal slices".The experiments reported that PBT2 was able to prevent synapatic toxicity or loss of signal conductivity, caused by the formation of toxic Aβ oligomers. The data indicates that it may be most beneficial for neuroprotective agents such as PBT2, that can interrupt Aβ self-assembly into aggregates, to be administered to early stage patients to best maintain synaptic plasticity and function as an effective treatment for Alzheimer's Disease (AD"
That was in murine(mouse)slices. There has to be more going on other than just very weak iron chelation IMO. There was possibly mitochondria recovery as well. Probably the dose was too low in the trials, and PBT434 combination may have made the difference if there is synergy between those two MPACs.
