NEW YORK, Nov. 23, 2016 /PRNewswire/ -- Neurotrope, Inc. (OTCQB: NTRP), a company focused on developing drugs to treat neurodegenerative diseases including Alzheimer's disease, today issued a statement on Eli Lilly's experimental drug solanezumab. Lilly stated that, based upon results from its recent Phase 3 clinical trial, solanezumab failed to improve cognition of patients with mild Alzheimer's disease. Dr. Daniel Alkon, Neurotrope's President and Chief Scientific Officer stated' "I deeply regret the news released today that Lilly's latest trial of its leading Alzheimer's drug candidate has failed. Lilly's dedication and persistence to finding a cure for this devastating affliction deserves everyone's admiration and gratitude. Repeated attempts to treat or even slow the relentless progression of Alzheimer's disease by targeting the red flag in patient's brains called amyloid plaques have continued to lead to such disappointing outcomes. Neurotrope has focused all of its resources on regenerative medicine that would replace the lost synaptic networks that are so consistently associated with the breakdown of human cognitive functions. Bryostatin, a drug that induces growth of new networks to replace those that have degenerated while also degrading plaques and tau tangles, may also address the red flags of this scourge threatening increasing numbers of the world's aging populations. At Neurotrope, we believe that treating Alzheimer's disease is a daunting challenge that will need to be treated by a drug with multi modal efficacy. We believe that our drug bryotstatin may be the drug. The top line results of our Phase 2 study with 148 patients is expected to be announced in April 2017. We hope, at that time, that a new therapy will be viewed as a possible future treatment for this disease." About Neurotrope Neurotrope BioScience, Inc., a wholly owned subsidiary of Neurotrope, Inc., 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 e and a by bryostatin, a natural product, which in mouse AD models was demonstrated to result in repair of damaged synapses as well as synaptogenesis, the induction of new neuronal networks, reduction of toxic beta-amyloid generation, prevention of neuronal death, and enhancement of memory and learning, thus having the potential to improve cognition and behavior in Alzheimer's disease.