Sorry forgot this bit
Tanzi on the mouse study:
“In my view, these data help explain why other Alzheimer's therapies that solely target Abeta or tau pathology may, at best, be only partially effective. PBT2, by addressing metal induced oligomer formation, restoring metal balance in affected brain regions, and by promoting new neuronal cell growth, elicits a distinct set of disease modifying effects. Thus PBT2 may not only ameliorate Alzheimers pathology, but perhaps other detrimental aspects of aging on the brain”, concluded Dr Tanzi.
PBT2 restored learning and memory. The old mice treated with PBT2 performed learning and memory tasks to the same level exhibited by young mice and significantly better than untreated old mice (p<.01 or better).
PBT2 Increases markers of neurogenesis and neuron number:
a) Increased number of mature neurons by up to 27% in the hippocampus
b) Increased markers of cell proliferation by 67% and markers of numbers of immature neurons by 130% in the hippocampus.
c) Neuronal proliferation markers were elevated around the lateral ventricles by 214% (atrophy of peri-ventricular tissue is a feature of Huntington’s disease)
PBT2 increases numbers of synapses in the hippocampus:
a) Synaptophysin levels increased by 38%
b) Dendritic spine density increased by 15%
PBT2 increases glutamate receptor levels in the hippocampus:
a) NMDA R2b levels increased by 88%
b) AMPA levels increased by 97%
PBT2 increases Protein Phosphotase 2a (PP2a) in the hippocampus:
a) PP2a increased by 22%
b) Phosphorylated Tau levels decreased by 81%
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