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NeuroSense Therapeutics & Massachusetts General Hospital's NeuroEpigenetics Lab to Collaborate on Elucidating Neurotherapeutic Effects of PrimeC in ALS
In vitro studies to test the effects of PrimeC on key pathways involved in ALS including TDP-43 accumulation, autophagy defects, mitochondrial dysfunction,
About this update from Neurosense Therapeutics Ltd.
[{"type":"text","content":"In vitro studies to test the effects of PrimeC on key pathways involved in ALS including TDP-43 accumulation, autophagy defects, mitochondrial dysfunction, and oxidative stressPreliminary results from this collaboration will be presented by Dr. Zimri at the upcoming AD/PD 2023 Advances in Science & Therapy Conference PrimeC is currently being evaluated in PARADIGM, a Phase 2b ALS trialCAMBRIDGE, Mass., March 27, 2023 /PRNewswire/ -- NeuroSense Therapeutics Ltd. (Nasdaq: NRSN) (\"NeuroSense\"), a company developing treatments for severe neurodegenerative diseases, today announced it has signed a collaboration agreement with Dr. Ghazaleh Sadri-Vakili, MS, PhD and Massachusetts General Hospital's NeuroEpigenetics Lab to explore the neurotherapeutic effects of its lead combination drug, PrimeC, utilizing a novel in vitro model generated from post-mortem ALS brain tissue (synaptoneurosomes (SNs) system).\n \nDr. Sadri-Vakili, Associate Professor at Harvard Medical School and the Director of the NeuroEpigenetics laboratory at the MassGeneral Institute for Neurodegenerative Disease, focuses on understanding the mechanisms involved in neurological disorders. Dr. Sadri-Vakili's laboratory has identified disease specific alterations in multiple cellular pathways using human samples as well as cellular and animal models of amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and X-linked dystonia-parkinsonism (XDP). In ALS, the laboratory is assessing the pathogenic role of neuroinflammation and oxidative stress using post-mortem samples. Key elements of these studies have recently been published using a novel ALS SNs system.\nThe objective of the collaborative studies is to expand the understanding of PrimeC's mechanism of action in attenuating ALS-related pathology, specifically TDP-43 accumulation, autophagy defects, mitochondrial dysfunction, and oxidative stress. To address this, ALS- or control-SNs derived from post-mortem brains will be used to treat SH-SY5Y cells to induce reactive oxygen species and mitochondrial dysfunction, as previously shown by the Sadri-Vakili lab, in the presence or absence of PrimeC. Importantly, the studies will compare the potential therapeutic effect of PrimeC combination therapy relative to each one of its FDA-approved compounds, ciprofloxacin and celecoxib, separately, to further demonstrate...