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Independent Study Corroborates Prana's Strategy to Treat Alzheimer's Disease Patients.
Date:4/1/2009

- Journal of Neuroscience paper describes role of Zinc in developing Alzheimer's -

MELBOURNE, Australia, April 1 /PRNewswire-FirstCall/ -- Prana Biotechnology (ASX:PBT; Nasdaq: PRAN) today announced that an independent study conducted by researchers at the University of California, Irvine, validates Prana's fundamental drug strategy for Alzheimer's Disease in blocking the toxic interaction between Abeta and brain metals, such as zinc, that damages synapses and cause cognitive loss.

The study, published in the Journal of Neuroscience showed that the release of zinc from synapses is critical for Abeta to form oligomers and to aggregate. Dr Glabe, an author of the paper, noted, "These results are very exciting news for understanding the mechanism of Alzheimer pathogenesis. They help elucidate the fundamental role of metal ions like zinc in causing the formation of Abeta oligomers which damage synapses".

Prana's lead Alzheimer's disease compound, PBT2, targets a toxic form of the Abeta protein in the synapses of the brain by inhibiting the interaction between Abeta and zinc. The findings provide an explanation as to how PBT2 has demonstrated the ability to restore normal function to Abeta-impaired synapses and so reverse cognitive loss in animal models of AD. PBT2 has completed a Phase IIa study in Alzheimer's disease patients, demonstrating a lowering of Abeta levels in the CSF and signs of cognitive improvement within three months.

Commenting on the significance of these findings Dr Jeffrey Cummings of UCLA, and Chair of Prana's Scientific Advisory Board, noted that, "the role of Abeta oligomers in damaging synapses resulting in cognitive impairment is well established in the literature. What has been less clear is why oligomers congregate at the synapse. The work by Dr. G
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