PRAN > Prana's PBT2 may clear amyloid-beta for Phase II Alzheimer's success though relevance questioned - experts
PBT2 will likely prove to be efficacious in this study as it shifts the balance of copper from the amyloid plaques to inside the neuron, inhibiting aggregation, agreed both Dr George Brewer, University of Michigan Medical School, and Peter Faller, professor of chemistry, University of Toulouse, France.
The first Phase II study was very encouraging, said laureate Professor Colin Masters, Mental Health Research Institute, Australia, and advisor to Prana. The data showed copper may be important for the initiation of aggregation of amyloid-beta and PBT2 can play a role in disrupting this, he said. Demonstration of reduction of amyloid-beta should be sufficient to move forward into Phase III, he added.
Relevance of primary endpoint questioned
Whilst a focus of the Phase II study, there is still uncertainty over the role of amyloid-beta in AD and whether its clearance is useful in overall treatment of the condition, experts agreed.
Despite reporting a significant decline in beta-amyloid in CSF in Phase IIa, it is currently unknown what the importance of that is, said Dr Gal Bitan, professor of Neurology, David Geffen School of Medicine, University of California at Los Angeles. The relevance of this biomarker is heavily debated, he said, noting lowering the amyloid-beta in the CSF may even increase amyloid-beta in the brain.
At the moment it just isn't known if amyloid-beta is causative to AD, said Porsteinsson. There are elderly patients with significant amyloid-beta deposition in the brain who display no symptoms of AD, thus its relationship to AD causality remains unknown, added Dr Mike Williams, adjunct professor in Molecular Pharmacology and Biological Chemistry Feinberg School of Medicine, Chicago, Illinois
Amyloid-beta likely has some role in the pathogenesis of the disease but whether this is a primary effect is not clear, noted Porsteinsson. It may be possible that elevation of amyloid-beta occurs in response to the disease as the body's natural compensatory mechanism, as this may be amyloid's normal function as a protein, but this is currently unknown, said Porsteinsson
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