A short scientific history

Since its founding as a private company in 1997 in Melbourne Australia, Prana has developed a unique platform technology in association with internationally recognized scientists and academic institutions, including:

• The University of Melbourne
• Massachusetts General Hospital, Boston MA
• The Mental Health Research Institute of Victoria

The company's research collaborators also extend to:

• The Buck Institute for Age Research, Novato, CA
• University of California, San Francisco, CA
• University College, London

The development of Prana's library of Metal-Protein Attenuating Compounds ('MPACs') commenced with the observation that Prana's first proof-of-concept MPAC - clioquinol ('PBT1'), abolished Alzheimer's-like changes in the brains of genetically engineered mice. Subsequent work demonstrated a significant reduction in cognitive decline in a pilot phase IIa study in Alzheimer's patients receiving PBT1. Due to an unrectifiable manufacturing impurity, PBT1 was retired and immediately succeeded by an improved and novel MPAC – 'PBT2' , the leading candidate to arise out of Prana's unique drug discovery platform. PBT2, while sharing a similar mechanism of action to PBT1, demonstrates superior technical and medicinal properties.

During the course of the development of MPACs, numerous papers from independent laboratories appeared in the scientific press, demonstrating the potential benefits of PBT1 over a broad range of human diseases, notably Parkinson's, Huntington's and certain cancers. In addition, the elucidation by Prana scientists of a toxic biochemical pathway in Alzheimer's Disease has revealed a novel target for a vaccine therapy.

Scientific model

Since 1994, Prana scientists have contributed to over 100 peer-reviewed, high impact publications demonstrating how subtle defects in the metabolism of trace biological metals lie at the core of common neurodegenerative conditions. For Alzheimer's Disease (AD) in particular, this theory provides an elegant and consistent explanation for many of the otherwise disparate pathological phenomena associated with this condition.

These include:

• Why the amyloid Abeta protein is deposited only in the brain when it is made by all tissues of the body.
• Why Abeta, an otherwise benign protein, can become toxic.
• How toxic aggregates (oligomers) form.
• Why pervasive oxidative damage is present in the brains of AD sufferers.
• Why some species (such as mice and rats) do not get the disease and why females of all species seem to be more susceptible.
• Why Apo E4 is a risk factor for developing Alzheimer's Disease

While the principle of metal-mediated oxidative damage has broad relevance across a range of age-related neurodegenerative disorders, such damage is also observed in a diverse range of conditions and this suggests applicability of Prana MPAC's to a variety of further diseases.