Metal Hypothesis for Alzheimer’s, Huntington and other Neurodegenerative Diseases Declared Promising Therapeutic Strategy by Scientists at New York Academy of Sciences Symposium

Melbourne – December 6th, 2012; Prana Biotechnology (NASDAQ:PRAN; ASX:PBT) today announced that leading scientists discussing the Metal Hypothesis at the New York Academy of Sciences on November 29th at a symposium titled “Targeting Metals in Alzheimer’s and Other Neurodegenerative Diseases”, highlighted the promise that therapies like Prana’s PBT2 could offer for sufferers of neurodegenerative diseases.

This symposium examined findings that have led to the discovery of small molecules designed to restore the balance of transition metals in the brain that are critical for normal neuronal function, that reduce the accumulation of aggregated target proteins associated with disease, and that could have a disease-modifying effect.

Dr. Rudy Tanzi, the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Prana’s Chief Scientific Advisor, said, “Researchers are increasingly focusing on the role of metals in neurodegenerative disease, providing data that promotes optimism for the outcome of Prana’s trials. As we learn more about the genetics of Alzheimer’s Disease it increasingly appears that the disease is triggered by the excessive accumulation of the amyloid beta protein in the brain. Prana’s therapeutic strategy for treating neurodegenerative disease involves a highly differentiated mechanism of action as an anti-beta-amyloid drug therapy”. Rather than simply trying to stop production of all native amyloid beta protein, PBT2 (i) prevents the metal dependent conversion of amyloid beta protein into oligomers that are toxic to synapses and (ii) restores normal brain metal distribution that is essential for neuronal health and synaptic function.

Dr. Steven M. Hersch, of Massachusetts General Hospital and Harvard Medical School said, “Transition metals, especially iron and copper, have been implicated in the pathogenesis of Huntington disease. Copper may directly modulate the toxicity of the huntingtin protein (Htt) while iron accumulation in response to neurodegeneration likely potentiates the damage to the central nervous system, making both metals potential therapeutic targets. PBT2 is the first clinical candidate that modulates Htt directly.”

Dr. Dan Tardiff, of the Whitehead Institute for Biomedical Research, said, “We have screened multiple validated yeast cells of proteotoxicity and identified numerous compounds that restore protein homeostasis and rescue cells from death. We have several compounds that rescue cell death through altering metal homeostasis. Though it is not clear the precise mechanism in some cases, it is becoming more apparent that, along with molecules like PBT2, targeting metals may ultimately be a productive therapeutic strategy in several neurodegenerative diseases.”

The presentations explored the causative events leading to the neuropathology that drives Alzheimer’s Disease, Parkinson’s Disease and Huntington Disease. Dr. Robert Cherny of The Florey Institute of Neuroscience and Mental Health, Melbourne, and Prana’s Head of Research, said, “We have been investigating the therapeutic potential of drugs which act to inhibit pathological metal-protein interactions and promote neuronal function by restoring metal homeostasis. We believe that cognition can be improved significantly with drugs like PBT2.”