Researchers from Insmed Inc. presented findings on INM-901, a novel synthetic cannabinoid analogue, demonstrating its effects in the 5xFAD mouse model of Alzheimer’s disease. Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive decline and sensorimotor impairments, with no available treatments that effectively halt disease progression.

Intracerebral hemorrhage accounts for 10%-15% of all cases of stroke, and it is associated with particularly poor prognosis due to primary and secondary brain injury driven by neuroinflammation. This inflammation involves the activation and subsequent pyroptosis, or lytic cell death, of microglia.

Chitinase-3-like protein 1 (CHI3L1) is a secretory glycoprotein from the glycoside involved in the regulation of immune and inflammatory responses. In the brain, CHI3L1 is primarily produced by activated astrocytes, where it is involved in inflammatory neurotoxicity, emerging as a potential biomarker of neuroinflammatory disorders, such as Alzheimer’s disease.

An experimental gene therapy based on the prime editing technique could become an effective treatment for alternating hemiplegia of childhood, a severe and currently incurable rare disease. David Liu’s lab at the Broad Institute, the inventor of this gene edition methodology, together with scientists from The Jackson Laboratory, successfully reversed the effects of five mutations associated with this disorder in a mouse model.

Researchers from Biotiche Drug Discovery Srl and collaborators have discovered that modulating the activity of a specific family of potassium channels, known as Kv3 channels, can have beneficial effects on the progression of amyotrophic lateral sclerosis (ALS) in a mouse model of the disease. The study, published in the journal Acta Neuropathologica Communications, provides new insights into the role of these channels in skeletal muscle function and their potential as a therapeutic target for ALS.