Adlard in 2013 shows how PBT2 is the anti-aging holy grail and this is why Tanzi likens PBT2 to a statin
A novel approach to rapidly prevent age-related cognitive decline
Paul A. Adlard, et al
Summary
The loss of cognitive function is a pervasive and often debilitating feature of the aging process for which there are no effective therapeutics. We hypothesized that a novel metal chaperone (PBT2; Prana Biotechnology, Parkville, Victoria, Australia) would enhance cognition in aged rodents. We show here that PBT2 rapidly improves the performance of aged C57Bl/6 mice in the Morris water maze, concomitant with increases in dendritic spine density, hippocampal neuron number and markers of neurogenesis. There were also increased levels of specific glutamate receptors (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and N-methyl-d-aspartate), the glutamate transporter (VGLUT1) and glutamate itself. Markers of synaptic plasticity [calmodulin-dependent protein kinase II (CaMKII) and phosphorylated CaMKII, CREB, synaptophysin] were also increased following PBT2 treatment. We also demonstrate that PBT2 treatment results in a subregion-specific increase in hippocampal zinc, which is increasingly recognized as a potent neuromodulator. These data demonstrate that metal chaperones are a novel approach to the treatment of age-related cognitive decline.
Kad repost:
"Then big news came from a study in Australia, where they tracked amyloid in people’s brains — people who were unaffected and people who had the disease.
What came out of that study was that amyloid accumulates in the brain 15 years before symptoms. So in these trials, you’re treating full-blown Alzheimer’s patients for amyloid, but amyloid had already accumulated, started the disease, and done its job."
"I also have two drugs in clinical trials. One, that stops the amyloid from aggregating, is called PBT2, from Prana Biotechnology, a company I founded in my lab. That drug aims to stop the aggregation of the amyloid in the brain so it can clear out. "
Now if amyloid build up is the cause, beginning 15 years before onset of AD, and PBT2 can prevent the build up by clearing soluble oligomers, why is Prana not considering a short trial to prove PBT2 does work like a statin, for approval?
The first Lipitor approval was based on 4 trials
Ascot,
Between February 1998 and May 2000, a total of 19,341 patients in Denmark, Finland, Iceland, Ireland, Norway, Sweden, and the United Kingdom were enrolled into ASCOT
Cards,
A total of 2838 patients from 132 centers in Ireland and the UK were randomized, with mean LDL levels at baseline of 118 mg/dL in the atorvastatin group and 119 mg/dL in the placebo group.
TNT
The TNT trial is a parallel-group study randomizing 10 001 patients from 14 countries to a double-blind treatment with either atorvastatin 10 mg or 80 mg.
IDEAL
The Incremental Decrease in Endpoints Through Aggressive Lipid Lowering (IDEAL) study evaluated Lipitor 80 mg/day compared to simvastatin 20 to 40 mg/day in 8,888 subjects up to 80 years of age with a history of CHD to assess whether reduction in CV risk could be achieved.
OK so there is no time to treat AD plaques early then look for outcomes 15 ears later. I would say they should be trying to replicate the reduction of soluble oligomers again for approval as a AB Statin.
kadaicher1 • 7 hours ago Flag
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Interesting the up regulation of zinc in the hippocampus ties in with this Korean research,
"Clioquinol induces autophagy in cultured astrocytes and neurons by acting as a zinc ionophore"
which ties in with the thrust of the paper you just posted.
"Degradation of misfolded proteins by autophagy: is it a strategy for Huntington's disease treatment?"
I get the feeling the science behind the HD program is almost watertight.
The Htt signal seen in the Reach2HD trial suggests the scientists who completed that research above have already had their work validated in a human trial.
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