new key findings, page-2

Prana presents new findings on lead Alzheimer's drug
09:29, Thursday, 7 June 2007

Sydney - Thursday - June 7: (RWE Australian Business News) -
Prana Biotechnology Ltd (ASX code: PBT), a biopharmaceutical company
focused on research and development of treatments for neurodegenerative
disorders, announced today it would present new data on Prana's lead
Alzheimer's disease (AD) drug, PBT2, at the Alzheimer's Association
International Conference on Prevention of Dementia, in Washington DC.
Professor Colin Masters, executive director and Laureate
Professor Mental Health Research Institute and The National Neuroscience
Facility University of Melbourne and director of the company, will
present the findings on June 9, in a lecture entitled "Alzheimer's
Disease: Abeta amyloid as the principal molecular therapeutic and
diagnostic target".
The presentation will include data from manuscripts currently
under preparation for publication by scientists from Prana, The Mental
Health Research Institute and The University of Melbourne.

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While PBT2 is currently in Phase IIa development, the
presentation will detail the results of the expansive mouse cognitive
and biomarker studies recently completed on PBT2, including several key
findings such as:
* PBT2 potently inhibits synthetic Abeta forming toxic soluble
oligomers in vitro;
* PBT2 reduces Abeta oligomer levels detected in secretions
from the brains of conscious, freely-moving AD transgenic mice within
four hours of oral administration. This observation was reproduced in
two genetically distinct mouse models.
* PBT2 sharply improves cognitive performance in the Morris
Water Maze for two genetically distinct mouse models of AD within five
to seven days of treatment; and
* the brains of the mice with improved cognition showed a
substantial reduction in the biomarkers phosphorylated tau and Abeta,
while simultaneously raising the level of the neuronal marker protein
synaptophysin.
The amyloid plaques which are the main pathological feature of
the brains of Alzheimer's sufferers are composed of aggregates of the
Abeta protein.
The Alzheimer's research community largely supports the
hypothesis that small, soluble, mobile aggregates (oligomers) of the
Abeta protein are the cause of neurotoxicity in AD.
PBT2's ability to inhibit the generation and toxicity of these
oligomers, as well as preventing the hyperphosphorylation of tau, while
improving cognition, supports the disease modifying potential of PBT2
and other drugs in the Prana development pipeline.