Acurastem Inc. has raised nearly $7 million in grant funding from the National Institutes of Health (NIH) and the Department of Defense (DoD) to advance research in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia.
Coya Therapeutics Inc. intends to expand proposed indications for COYA-302 beyond amyotrophic lateral sclerosis (ALS) to include frontotemporal dementia (FTD) and Parkinson’s disease.
4D Molecular Therapeutics Inc. (4DMT) and Arbor Biotechnologies Inc. have established a strategic partnership focused on advancing new AAV-based gene-editing therapies for central nervous system (CNS) diseases with high unmet medical need in both rare and common disease populations.
Sudo Biosciences Inc. has closed a $116 million series B financing, with the funding raised to be used to advance two investigational TYK2 candidates into the clinic in 2024.
Researchers from West China Hospital of Sichuan University presented data from a study that aimed to investigate the associations between serum cystatin C (CysC) levels and the progression and survival of patients with amyotrophic lateral sclerosis (ALS).
Merck Sharp & Dohme LLC has identified receptor-interacting serine/threonine-protein kinase 1 (RIPK1; RIP-1) inhibitors reported to be useful for the treatment of amyotrophic lateral sclerosis and inflammatory disorders.
University of Oxford scientists have presented data from deep proteomics of cerebrospinal fluid (CSF) in search of proteins with diagnostic or prognostic value in amyotrophic lateral sclerosis (ALS). Analysis was performed using CSF samples from 40 ALS patients, 15 controls (healthy individuals) and 8 mimicking conditions.
Microtubule acetylation and impaired axonal transport have been proposed as mechanisms causing amyotrophic lateral sclerosis (ALS). Furthermore, histone deacetylase 6 (HDAC6) is known to play a role in acetylation of α-tubulin, a subunit of microtubules. ACY-738 is an HDAC6 inhibitor that has been reported to slow neuron degeneration in Alzheimer’s disease and ALS models by increasing acetylation of α-tubulin.
