AB Science announced the publication of new preclinical results for masitinib in neurodegenerative diseases. Findings have been published on the bioRxiv preprint service as an article entitled, ‘Masitinib limits neuronal damage, as measured by serum neurofilament light chain concentration, in a model of neuroimmune-driven neurodegenerative disease’. This article is freely accessible online from the bioRxiv site. The neuroprotective action of masitinib was studied in an animal model of experimental autoimmune encephalitis. EAE is a model of neuroimmune-driven chronic neuroinflammation and importantly, neuronal damage, or prevention thereof, can be rapidly assessed by measuring serum neurofilament light chain concentration in EAE-induced mice. Results showed that masitinib can significantly lower serum NfL levels, and by extension therefore, neuronal damage, in a neuroimmune-driven neurodegenerative disease model, with concomitant reduction in pro-inflammatory cytokines and slowing of clinical symptoms. Key points from this research article include: Masitinib treatment significantly limited NfL production in EAE mice with respect to the control group, at various timepoints during the 15-day treatment period and in a dose dependent manner. Masitinib significantly lowered several well-established pro-inflammatory cytokine biomarker concentrations in EAE mice. A beneficial effect of masitinib on functional performance was also observed, with significantly less relative deterioration in grip strength as compared with the control group. The measurement of NfL in biological fluids has been proposed for monitoring the therapeutic effect of drugs aimed at reducing axonal damage in various NDDs, including amyotrophic lateral sclerosis, multiple sclerosis, and Alzheimer’s disease. EAE is a model of neuroimmune-driven chronic neuroinflammation and therefore highly relevant to masitinib’s mechanism of action in NDDs. Data was derived after disease onset, which is of greater relevance because such models more closely simulate the clinical condition of NDD patients and therefore better represent their therapeutic needs.
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