Prana's PBT2 Reverses Memory Loss in Normal Aging

MELBOURNE, AUSTRALIA--(Marketwired - Oct 30, 2013) - Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN),

• PBT2 Increases numbers of Neurons in the brain
• PBT2 increases numbers of Synapses in the brain
• PBT2 increases NMDA and AMPA levels
• PBT2 increases Protein Phosphatase 2a (PP2a)

Prana Biotechnology (ASX: PBT) (NASDAQ: PRAN), a leading global developer of first-in-class treatments for neurodegenerative disease, has today announced the publication of an article in the peer reviewed Aging Cell showing the effects of PBT2 on neurogenesis and in reversing the memory and learning losses associated with the aging process, in normal (ie non transgenic) old mice.

The paper, entitled "A Novel Approach To Rapidly Prevent Age-Related Cognitive Decline", appears in the journal Aging Cell available now online here*. The authors were led by Associate Professor Paul Adlard, Head, Synaptic Neurobiology Laboratory, The Florey Institute of Neuroscience and Mental Health.

"It is very exciting to discover that PBT2 not only helps clear amyloid from the brain, but is promoting the birth of new nerve cells in a part of the brain that is particularly affected by Alzheimer's disease, the hippocampus. This now adds to the predicted beneficial properties of PBT2 for the treatment and prevention of Alzheimer's disease," commented Dr Rudy Tanzi, Professor of Neurology at Harvard Medical School, Vice Chair of Neurology at Massachusetts General Hospital, and Prana's Chief Scientific Advisor.

Age-related cognitive decline occurs in humans along with all other mammals. Data in this publication, describes how PBT2 reversed both memory and cognitive loss in aged mice.

Previously Prana reported the positive effects of PBT2 on increasing neuronal number, synaptic density and up regulation of critical markers of synaptic function and plasticity in an transgenic animal model of Alzheimer's disease, as well as significantly improved cognition (see Prana press release 21 March 2011 here). These new findings are in normal old mice that have not been genetically modified and do not form amyloid.