The Blanchette Rockefeller Neurosciences Institute (BRNI) at West Virginia University will be working with Alzheimer’s disease-focused, Florida-based biotech company Neurotrope BioScience to advance novel diagnostic and therapeutic technologies developed at BRNI that have shown promise in both preclinical and clinical models of Alzheimer’s.
The first milestone they’ll be seeking is the commercial introduction in the 2014 timeframe of a new, noninvasive diagnostic test for early-stage Alzheimer’s disease. Following this, the BRNI-Neurotrope BioScience team will be initiating several Phase II clinical trials in Alzheimer’s with drug prototypes discovered at BRNI. The first commercial introduction of one of these experimental medicines could occur in 2018.
BRNI and Neurotrope BioScience claim the scope of this effort is unprecedented and will involve ongoing contributions from BRNI research personnel and other resources within the state of West Virginia. They also say that the effort presages an entirely different concept on what causes Alzheimer’s disease and how to treat its ravaging effects.
“We are incredibly excited to advance the scientific discoveries at BRNI into mid-stage clinical trials where we intend to investigate our drug prototypes in not only Alzheimer’s disease, but also ischemic stroke and Fragile X syndrome,” said Daniel Alkon, M.D., scientific director at BRNI, who will be taking on the role of CSO of Neurotrope BioScience.
“It takes on average, 12 to 15 years for a new medicine to gain FDA approval and reach the bedside of a patient who needs it,” said Lane Bailey, chairman of the BRNI board of directors. “We are all grateful for this new investment that will allow BRNI’s scientists to build on their progress and showcase the kind of research and advancement underway in the Mountain State.”
What kind of research and advancement? In March of 2012, BRNI researchers reported in a paper in the Journal of Biological Chemistry that they found that the normal ApoE3 gene stimulates the growth of synapses through a protein called PKC epsilon, which also prevents the toxic Alzheimer’s disease protein, beta amyloid, from destroying synapses. ApoE4, a defective version of the ApoE gene, could cause the early loss of synapses in Alzheimer’s disease by not stimulating the synthesis of PKC epilson, they said. Also, in January of 2011, a BRNI study published in the Journal of Neuroscience reportedly revealed underlying causes for the degeneration of synapses in Alzheimer’s disease and identifed potential pharmaceutical solutions for the disease. BRNI claims that the study was the first to achieve fundamental molecular understanding of how synapses are lost in Alzheimer’s disease before the plaques and tangles develop.
