Neurotrope announces that a new study published in the Journal of Biological Chemistry shows that Bryostatin, a PKC epsilon Activator, Generates New Synapses Through Accumulation of the Synaptic Anchoring Protein PSD-95 at Neuronal Membranes
PR NewswireJune 23, 2016
NEWARK, N.J., June 23, 2016 /PRNewswire/ -- Neurotrope, Inc. (NTRP) today announced that a study published in the Journal of Biological Chemistry shows that its lead Alzheimer's drug, Bryostatin, licensed from the Blanchette Rockefeller Neurosciences Institute (BRNI), increases the levels of the synaptic scaffolding protein PSD-95, and induces the movement of phosphorylated PSD-95 to the neuronal membranes.
The study, conducted within the BRNI basic research programs, showed that Bryostatin induced activation of PKC epsilon increased synaptic number, pre-synaptic vesicle density, and clusters of PSD-95. It is known that either Aß or tau, both toxic proteins in Alzheimer's disease brains, can induce reduction of PSD-95 in excitatory synapses in hippocampus. Furthermore, this PSD-95 reduction continues to occur as the Alzheimer's pathologies advance. A Phase 2b clinical trial funded by Neurotrope Bioscience, Inc., Neurotrope, Inc.'s wholly-owned subsidiary, is underway to test the efficacy of Bryostatin for the treatment of the causes and progression of Alzheimer's disease.
The new study, demonstrating for the first time a close relationship between PKC epsilon and its downstream target, PSD-95, is entitled "PKC epsilon Promotes Synaptogenesis through Membrane accumulation of the Postsynaptic Density Protein PSD-95" with lead author, Dr. Abhik Sen, as published online in the Journal of Biological Chemistry, June 21, 2016. "Dr. Sen, together with Dr. Tom Nelson, continue to reveal important new insights into the processes of brain degeneration and regeneration," said Dr. Dan Alkon, Scientific Director of BRNI.
"Our studies consistently demonstrate that the synaptogenic growth factors such as BDNF, NGF, IGF, etc. are increased by bryostatin-induced activation of PKC epsilon. Bryostatin has the ability to regenerate the brain wiring lost in pre-clinical disease models and entirely restore memory capacity due to many causes of neurodegeneration such as Alzheimer's, Fragile X, and TBI." Dr. Alkon went on to say, "This latest article provides major new evidence that BRNI is developing and Neurotrope is clinically testing bryostatin as a potential "universal" therapeutic for neurodegeneration in the brain, however it arises, even due to disease genes as distinct as Fragile X, ApoE, and Presenilin – as recently described in a BRNI review article published in the June 2015 edition of Trends in Pharmacological Sciences (Vol. 36 No. 6. http://dx.doi.org/10.1016/j.tips.2015.04.004)."
Neurotrope, Inc. is currently conducting a Phase 2B clinical trial to validate PKC epsilon activation therapy in Alzheimer's disease, a potential paradigm shift in the field, for which Bryostatin already has received Orphan Drug status from the FDA for Fragile X Syndrome (FRX).
http://finance.yahoo.com/news/neurotrope-announces-study-published-journal-123000681.html
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