Treatment with masitinib was shown to prevent the amyloid-induced hemichannel-dependent mast cell activity in bone marrow-derived mast cells and brain mast cells.
Phillip Scheltens, MD
Masitinib’s ability to block hemichannels (HCs) on mast cells (MCs) pose as a promising novel strategy for slowing the progression of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer disease (AD), according to a recently published peer-reviewed study.1,2
The independent publication was led by Paloma A. Harcha, PhD, post-doctoral researcher, University of Vaparaiso, exposes the fact that these HCs allow cell communication with the extracellular environment and have diverse and pathophysiological roles in the nervous system. The review article focuses on HCs formed by connexins (Cxs) and pannexins (Panxs) proteins and their contribution to MC degranulation in AD, ALS, and harmful stress conditions.
“This research provides further supportive evidence that masitinib, through its dual targeting of mast cells and microglia, has a unique and effective profile for neurodegenerative diseases such as Alzheimer’s disease and amyotrophic lateral sclerosis,” Phillip Scheltens, MD, professor of neurology, Alzheimer Center Amsterdam, said in a statement.
Masitinib, a tyrosine kinase inhibitor, has shown to decrease the number of MCs in the extensor digitorum longus (EDL), and reduces the rate of neuromuscular junction (NMJ) denervation and motor deficits in rats with the mutant SOD1 ALS gene. While it remains unclear how exactly masitinib targets skeletal muscle MCs in ALS, studies have shown that it inhibits migration and degranulation.
|
