Prana's Research Was Presented At International Conference On Alzheimer's Disease On July 14
Main Category: Alzheimer's / DementiaAlso Included In: Neurology / Neuroscience
Article Date: 20 Jul 2010 - 0:00 PDT
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Prana Biotechnology Limited (NASDAQ: PRAN) (ASX: PBT), Head of Research, Assoc. Prof. Robert Cherny, presented new data on PBT2, the Company's lead compound in development for Alzheimer's Disease on July 14th at the prestigious International Conference of Alzheimer's Disease (ICAD) in Honolulu. The presentation was entitled "Novel molecular mechanisms for the neurotrophic and neuroprotective effects of PBT2 in Alzheimer's Disease and Huntington's Disease." The presentation is now available on Prana's website.
ICAD 2010 drew thousands of international attendees to Hawaii to share the latest ideas, thoughts and theories in dementia science. Breaking research and new technology captured global media attention as the world's leading scientists explored innovative ways to unlock the mysteries of Alzheimer's.
The new findings presented by Prof. Cherny show that the effectiveness of PBT2 lies in a unique combination of complementary activities. PBT2 acts to detoxify A-beta by disarming it of copper and zinc and returns these crucial metals to neurons. Assoc. Prof. Cherny presented data* showing that by returning these metals to neurons, important cell signaling pathways are activated that prevent neuronal death and promote neuronal function. In addition, data was also presented linking the neuroprotective qualities of PBT2 with beneficial effects evident in an animal model of Huntington's Disease.
In collaboration with the University of California San Francisco, PBT2 was tested in the R6/2 transgenic model of Huntington's Disease. The mice exhibited significant improvement in coordination, motor function and lifespan**. Significantly, examination of the brains of treated mice showed marked reduction in atrophy of the striatal tissue. In Huntington's Disease, this tissue degenerates resulting in the loss of brain volume, a hallmark of the disease.
Professor Ashley Bush, a member of Prana's Research and Development Advisory Board, commented about the significance of the data that was presented at ICAD, "The evidence is growing rapidly that disorder regulation of brain metal metabolism underlies major neurological diseases, such as Alzheimer's, Parkinson's and Huntington's Diseases. Prana's drug approach elegantly targets abnormal metal distribution while leaving essential minerals alone. The strong benefits we've seen in animal testing, and the rapid improvement in the Phase 2 clinical trial of PBT2 for Alzheimer's Disease, indicate that this unique approach holds enormous promise."
*8 month old APP/PS1 mice were treated for 11 days oral PBT2 30 mg/kg (n=7) or vehicle (n=7), In the brains of drug treated animals statistically significant (P < 0.05) increases were detected in levels of neuronal markers TrkB, NMDAR1, NMDAr2a, NMDAR2b and CAMKII compared with untreated controls. Primary mouse cortical neurons cultured in the presence of 10µMPBT2 and 10µM zinc were protected against the toxic effects of 30µM glutamic acid (P < 0.01).
**R6/2 (transgenic HD) mice were administered 30mg/kg PBT2 orally (n=10) or vehicle (N=10) for up to 8 weeks. Significant improvements (P < 0.05) were observed in performance in the rotorod and hindlimb clasping tasks in the drug treated animals compared with the untreated controls. The average cumulative lifespan of the PBT2 treated animals was around 40% longer than that of the untreated controls (P < 0.05).
Source:
Prana Biotechnology Limited
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16 Feb. 2012. <http://www.medicalnewstoday.com/releases/195176.php>
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http://www.medicalnewstoday.com/releases/195176.php.
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