Alzheimer’s disease (AD) is a neurodegenerative disease and the major cause of impaired memory affecting the older population. Reported cases are rapidly increasing. So far, clinical trials have failed to make a significant impact on AD patients’ memory.
In the past, the target has been neurotoxic amyloid-beta. However, as one researcher notes, while the amyloid-beta protein is found in the brains of AD patients, its pathogenic role is unknown.
A recent press release issued by Neurotrope Inc. quotes a publication emphasizing that the restoration of synaptic (nerve) functions should be a major therapeutic goal when treating AD patients.
The online publication entitled Trends in Pharmacological Sciences highlights the synaptic deficiency hypothesis. The synaptic hypothesis updates the twenty-year-old amyloid cascade hypothesis. The new theory is that amyloid is an effect and not the cause of Alzheimer’s disease. These reports are based on clinical trials that have been completed.
About Neurotrope
An overview of the publication sets out previous nonpharmacological treatments. It also references Neurotrope’s Bryostatin that targets synaptic functions, improves cognitive functions in AD-related impairment, and prevents neuronal death.
Neurotrope Inc. is now conducting a Phase 2 trial of Bryostatin-1 based on clinical data from its earlier Phase 2 exploratory trial. The company expects to have trial results in the third quarter of 2019.
The FDA has granted Neurotrope an Orphan Drug Designation for Bryostatin-1. The designation is an incentive for further development of the drug in connection with Fragile X syndrome, a rare disorder.
Over 1500 people with cancer have been tested with Bryostatin-1. This has created an enormous database that can assist future designs for new clinical trials.
