Study shows bryostatin plays key role in slowing or reversing Alzheimer's disease

Neurotrope, Inc. (OTCQB: NTRP) today announced that results from a new study, entitled, "PKCe Deficits in Alzheimer's Disease Brains and Skin Fibroblasts," published in the recent edition of the peer-reviewed Journal of Alzheimer's Disease and co-authored by Tapan K. Khan, Ph.D.; Abhik Sen, Ph.D.; Jarin Hongpaisan, Ph.D.; Chol S. Lim, Ph.D.; Thomas J. Nelson, Ph.D., and; Dr. Daniel L. Alkon, each of the Blanchette Rockefeller Neurosciences Institute (BRNI), provide further indication of the role that protein kinase C epsilon (PKCe) may play in the potential treatment of Alzheimer's disease (AD). Neurotrope is currently collaborating with BRNI on the development of its lead compound, bryostatin, a potent modulator of PKCe, for the treatment of patients with AD.

A major hurdle in the treatment of AD is that patients only show symptoms years after the disease has already taken hold. Most treatments have focused on stimulating the neurotransmitter activity of healthy neurons in the brain, or removing the beta-amyloid plaque or tau protein which builds up in the brain as a result of the disease. All drug development efforts to date that have targeted the removal of beta-amyloid or tau protein, have failed, and drugs approved for stimulating neurotransmitter activity have offered only short-lived, palliative results for patients. Further, these treatment strategies have had no effect on the progression of the disease and have yielded no improvement in patients' memory or cognitive performance.

As reported in BRNI's recently published study, in brain samples (consisting of autopsy-confirmed AD and age- and gender-matched control samples), blindly provided by the Harvard Brain Bank, the amount of PKCe was found to be significantly reduced in specific areas of the brain that are known to be targets in early AD. In these same brain areas, the study also showed that levels of A Beta oligomers (a toxic protein formed as a result of AD) are elevated when PKCe is reduced. Remarkably similar changes were consistently found in the skin cells of AD patients when compared to their age-matched controls and as compared to patients with non-AD dementias (skin samples for the study were obtained from the cell bank at the Coriell Institute for Medical Research). Additionally, low levels of PKCe in skin cells were strongly correlated with progression of the disease. The longer the patients had AD, the lower their levels of PKCe. Further, low levels of PKCe in the brain were significantly correlated with an accepted measure of disease severity, known as the Braak score.

Taken together, these findings indicate that the presence of low levels of PKCe support the enzyme's potential value as an early therapeutic target in AD.

Dr. Alkon, Toyota Chair in Neurodegenerative Disease, Scientific Director and Professor, Blanchette Rockefeller Neurosciences Institute, and Chief Scientific Officer of Neurotrope, stated, "The results of this study are compelling and warrant continued research to fully explore the importance of PKCe in the identification and treatment of patients with AD. The data compiled from this study, and that related to Neurotrope's lead compound, bryostatin -- which, in preclinical in vivo models has shown to play an important role in slowing or reversing AD and restoring cognition, memory and motor skills -- provides additional incentive to pursue what could lead to a major shift in the medical community's approach to this debilitating and costly disease, which currently afflicts approximately 36 million people, worldwide."

Paul Freiman and Charles S. Ramat, Neurotrope's Co-Chairmen and Co-Chief Executive Officers, noted, "We believe that our Company's focus on modulating the levels of PKCe, instead of on the removal of beta-amyloid and tau protein, represents a novel, promising model for tackling what has been a highly frustrating and disappointing approach to treating this patient population. While still early stage, bryostatin has shown the potential to restore synaptic structures and functions damaged by AD, and as such, holds the promise of becoming a new, first-in-class treatment which may provide significant improvement in quality of life. The results of BRNI's most recent study, as published in the Journal of Alzheimer's Disease, lend additional credibility to our development of bryostatin which just recently entered a Phase 2a study." As previously announced, management expects to report a top-line analysis of the Phase 2a study by the end of the first quarter of 2015.

Messrs. Freiman and Ramat went on to say, "The potential for bryostatin goes beyond just the treatment of patients with AD. Due to the compound's ability to activate PKCe and to therefore stimulate the formation of new synaptic connections, the drug may have applicability to other neurodegenerative brain diseases, including patients suffering from traumatic brain injuries, stroke or mental retardation."