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      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

      Bryostatin, currently in a Phase 2b Alzheimer's Disease clinical trial, causes regeneration of synaptic networks in both Alzheimer's and Fragile X mouse models, neurodegenerative diseases at both ends of the age spectrum.


      News provided by

      Neurotrope, Inc.

      Jun 23, 2016, 08:30 ET

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      NEWARK, N.J., June  23, 2016 /PRNewswire/ -- Neurotrope, Inc. (OTCQB: 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 Aβ 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).

      About The Blanchette Rockefeller Neurosciences Institute
      Located in Morgantown, West Virginia, BRNI, at West Virginia University, is a unique, independent, non-profit institute dedicated to the study of memory and finding solutions to memory disorders. BRNI was founded in 1999 in memory of Blanchette Ferry Hooker Rockefeller, an Alzheimer's patient and mother of U.S. Senator John D. Rockefeller IV. BRNI is operated in alliance with West Virginia University.

      About Neurotrope
      Neurotrope BioScience, Inc., a wholly owned subsidiary of Neurotrope, Inc. (Neurotrope, or the Company), is at the forefront of biotechnology companies having a focus on developing a novel therapy for the treatment of moderately severe to severe Alzheimer's disease. The scientific basis of our treatment is activation of Protein Kinase C isozymes ε and α by bryostatin, a natural product, which can result in repair of damaged synapses as well as synaptogenesis, reduction of toxic amyloid generation, and enhancement of memory and learning, thus having the potential to improve cognition and behavior in Alzheimer's disease.

      Neurotrope is also conducting preclinical studies of bryostatin as a treatment for Fragile X Syndrome and Niemann-Pick Type C disease, two rare genetic diseases for which only symptomatic treatments are currently available. The Food and Drug Administration has granted Orphan Drug Designation to Neurotrope for bryostatin as a treatment for Fragile X Syndrome.  Bryostatin has undergone testing in over 1,400 people establishing a large safety database.

      Neurotrope has exclusively licensed technology from the Blanchette Rockefeller Neurosciences Institute for Alzheimer's disease and Fragile X Syndrome, and has a world-wide, exclusive license with the Icahn School of Medicine at Mt. Sinai for Niemann-Pick Type C.  Neurotrope has also entered into a collaboration with RettSydrome.org and is partnered with Stanford University to synthesize and find the next generation bryostatin – called bryologs.

      Forward-Looking Statements

      Any statements contained in this press release that do not describe historical facts may constitute forward-looking statements. These forward-looking statements include statements regarding the proposed study and timing of initiation, and continued development of use of bryostatin for Alzheimer's disease and other cognitive diseases.  Such forward-looking statements are subject to risks and uncertainties and other influences, many of which the Company has no control over. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements as a result of these risks and uncertainties. Factors that may influence or cause actual results to differ materially from expected or desired results may include, without limitation, the significant length of time associated with drug development and related insufficient cash flows and resulting illiquidity, the Company's patent portfolio, the Company's inability to expand the Company's business, the Company's inability to meet listing requirements for major stock exchanges, significant government regulation of pharmaceuticals and the healthcare industry, lack of product diversification, availability of the Company's raw materials, existing or increased competition,  stock volatility and illiquidity, and the Company's failure to implement the Company's business plans or strategies. These and other factors are identified and described in more detail in the Company's filings with the U.S. Securities and Exchange Commission, including the Company's Annual Report on Form 10-K for the year ended December 31, 2015 and Quarterly Report on Form 10-Q for the quarter ended March 31, 2016. The Company does not undertake to update these forward-looking statements.

      Please visit www.neurotropebioscience.com for further information.

      For additional information, please contact:
      Neurotrope Bioscience
      Charles Ramat, Chief Executive Officer
      973-242-0005
      [email protected]

      SOURCE Neurotrope, Inc.

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