Prana Biotechnology Ltd. has announced the publication of key research findings with its lead Alzheimer's Disease drug, PBT2.
The article titled "Rapid restoration of cognition in Alzheimer's transgenic mice with 8-hydroxyquinoline analogs" is associated with decreased interstitial Abeta" appears in the current edition of the prestigious scientific journal Neuron, and can be viewed online.
The key findings reported are:
- PBT2 profoundly and rapidly improved cognition in transgenic mice.
- PBT2 prevented the formation of soluble Abeta oligomers, the form of Abeta believed to be the most toxic.
- PBT2 substantially reduced the amount of all forms of Abeta in the transgenic mouse brain, over a nine week period.
- PBT2, within hours of oral administration, significantly lowered soluble (interstitial) Abeta in the brain, sampled using in vivo microdialysis.
- Using a well established model for memory formation, PBT2 protected neurons in living brain tissue from the toxic effects of Abeta which impairs the signaling between neurons in Alzheimer's disease.
"The Alzheimer's field is eagerly awaiting the results of several clinical trials of therapies aimed at the toxic amyloid beta protein. Prana's PBT2 is uniquely positioned as an oral drug that neutralizes the toxicity of the amyloid beta protein and clears it from the brain. The positive findings in Alzheimer's mouse models along with the encouraging results from the phase II clinical trial of PBT2 greatly strengthen my belief that this drug will ultimately be shown to slow down disease progress in Alzheimer's patients," commented Dr. Rudolph Tanzi, Professor of Neurology at Harvard University, and Director of the Genetics and Aging Research Unit at MassGeneral Institute for Neurodegenerative Diseases.
In their discussion, the authors explain that healthy brain function is dependent upon the tightly regulated movement of metals within and between neurons. They speculate that with aging this restraint may be loosened, rendering the brain vulnerable to oxidative stress and the pernicious effects of Abeta accumulation. In the article, multiple modes of action for PBT2 are proposed based on the drug's intrinsic ability to capture and transport metals in the brain. This property explains how PBT2: