The news was recently announced by Neurotrope, a pharmaceutical company collaborating with BRNI in the development of bryostatin, a potent modulator of PKCe, for the treatment of patients suffering with AD.
One of the big challenges in treating AD is the fact that patients typically start presenting with symptoms years after the disease is already present.
The majority of treatments for AD have focused on stimulating the neurotransmitter activity of healthy neurons in the brain and in the ablation of the beta-amyloid plaque and tau protein that form as a result of the disease. However, so far, developing drugs specifically targeted at removing beta-amyloid plaque or tau protein has not been successful, and the existing drugs that stimulate neurotransmitter activity have not had an effect in the progression of the disease or in memory or cognitive performance improvement.
In the recent study, entitled “PKCe Deficits in Alzheimer’s Disease Brains and Skin Fibroblasts“ and published in the Journal of Alzheimer’s Disease, the team of researchers examined brain samples of autopsy-confirmed AD patients and age-matched controls, alongside skin fibroblast samples from AD and non-AD dementia patients, to study the role of PKCe in the pathophysiology of AD while determining its possible use as an early AD-biomarker.
In these samples, provided by the Harvard Brain Bank, the amount of PKCe was significantly lower in the hippocampus and temporal pole areas of AD brains, known to be targets in early AD.
Furthermore, in the same brain areas, Aβ oligomer (a toxic protein resultant of AD) levels were significantly higher.
Skin samples obtained from the Coriell Institute for Medical Research showed very similar results between AD patients, controls, and non-AD dementias, with low PKCe levels strongly correlating with disease progression and disease severity, as measured in the Braak score.
“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,” said Dr. Daniel L. Alkon, Toyota Chair in Neurodegenerative Disease, Scientific Director and Professor, Blanchette Rockefeller Neurosciences Institute, and Chief Scientific Officer of Neurotrope in a recent press release. “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.”
Regarding the current bryostatin Phase 2a clinical trial, Paul Freiman and Charles S. Ramat, Neurotrope’s Co-Chairmen and Co-Chief Executive Officers, added in the same press release “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 this study lend additional credibility to our development of bryostatin which just recently entered a Phase 2a study.”
The results obtained demonstrate that the relationship between Aβ levels and PKCe is severely compromised in AD patients, and highlight the potential of using PKCe as an early therapeutic target in AD.
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