PBT2

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- PBT2 -

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Observations:

Prana's PBT2 -- Directly Restores Neurons Critical to Cognition
PLoS ONE Publication on PBT2 Consolidates the Underlying Mechanisms for the Preclinical and Clinical Benefits of PBT2 in Alzheimer's Disease
Press Release Source: Prana Biotechnology On Monday March 21, 2011, 11:30 am EDT
...It has previously been shown that PBT2 neutralises the toxicity of the Alzheimer's Abeta protein by preventing the formation of toxic aggregates or oligomers*. These new results further explain how PBT2 can achieve such rapid improvements in cognition: by liberating copper and zinc trapped in amyloid deposits and returning those essential metals to neurons, where they are needed for normal function...
http://finance.yahoo.com/news/Pranas-PBT2-Directly-Restores-iw-2656906997.html?x=0

Metal ionophore treatment restores dendritic spine density and synaptic protein levels in a mouse model of Alzheimer's disease.
Adlard PA, Bica L, White AR, Nurjono M, Filiz G, Crouch PJ, Donnelly PS, Cappai R, Finkelstein DI, Bush AI.
Oxidation Biology Laboratory, The Mental Health Research Institute, Parkville, Victoria, Australia.
PLoS One. 2011 Mar 11;6(3):e17669.

Abstract

We have previously demonstrated that brief treatment of APP transgenic mice with metal ionophores (PBT2, Prana Biotechnology) rapidly and markedly improves learning and memory. To understand the potential mechanisms of action underlying this phenomenon we examined hippocampal dendritic spine density, and the levels of key proteins involved in learning and memory, in young (4 months) and old (14 months) female Tg2576 mice following brief (11 days) oral treatment with PBT2 (30 mg/kg/d). Transgenic mice exhibited deficits in spine density compared to littermate controls that were significantly rescued by PBT2 treatment in both the young (+17%, p<0.001) and old (+32%, p<0.001) animals. There was no effect of PBT2 on spine density in the control animals. In the transgenic animals, PBT2 treatment also resulted in significant increases in brain levels of CamKII (+57%, p = 0.005), spinophilin (+37%, p = 0.04), NMDAR1A (+126%, p = 0.02), NMDAR2A (+70%, p = 0.05), pro-BDNF (+19%, p = 0.02) and BDNF (+19%, p = 0.04). While PBT2-treatment did not significantly alter neurite-length in vivo, it did increase neurite outgrowth (+200%, p = 0.006) in cultured cells, and this was abolished by co-incubation with the transition metal chelator, diamsar. These data suggest that PBT2 may affect multiple aspects of snaptic health/efficacy. In Alzheimer's disease therefore, PBT2 may restore the uptake of physiological metal ions trapped within extracellular β-amyloid aggregates that then induce biochemical and anatomical changes to improve cognitive function.
PMID: 21412423 [PubMed] PMCID: PMC3055881
http://www.ncbi.nlm.nih.gov/pubmed/21412423
Free article: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0017669

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