Prana Biotechnology Limited (NASDAQ: PRAN) (ASX: PBT) announced that its Head of Research, Assoc. Prof. Robert Cherny, will present new data on PBT2, the Company's lead compound in development for Alzheimer's disease, at the Hot Topics Therapeutics/Intervention session on July 14th at the International Conference of Alzheimer's Disease (ICAD) in Honolulu. The presentation is entitled "Novel molecular mechanisms for the neurotrophic and neuroprotective effects of PBT2 in Alzheimer's disease and Huntington's disease."

The new findings 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 will present 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 will be 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.

Prof. Rudy Tanzi, co-founding scientist of Prana and Professor of Neurology at Harvard University Medical School, said, "The ability of PBT2 to promote normal neuronal function and prevent degeneration of the brain tissue further indicates the disease modifying potential of PBT2."

"Prana's mission is to create a library of compounds that can offer therapies to treat neurodegenerative disorder of high unmet medical need. We are very excited about the potential opportunity to treat these two devastating neurodegenerative disorders," commented Geoffrey Kempler, Prana's CEO.

*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