G protein-biased agonists enhance opioid-induced analgesia by selectively avoiding β-arrestin-2 (βarr2) signaling, which has been associated with reduced efficacy and adverse effects. Similarly, directing neurotensin receptor 1 (NTSR1) signaling toward β-arrestin pathways may promote analgesia via alternative mechanisms while minimizing side effects linked to G protein activation.

CLN3 disease, also known as juvenile neuronal ceroid lipofuscinosis, is a rare neurodegenerative disorder affecting neuronopathic lysosomal storage that severely impacts the central nervous system while also inducing notable peripheral neuromuscular symptoms. Researchers from Washington University School of Medicine have demonstrated the potential of gene therapy for CLN3 disease.

Jocasta Neuroscience Inc. has raised $35 million in a series A financing to advance its lead asset, JN-0413, a proprietary formulation of the longevity protein α-Klotho, through phase I development. The company is targeting an IND submission for the fourth quarter of next year.

Sareum Holdings plc has entered into a strategic collaboration with Receptor.AI Ltd. to accelerate the discovery and optimization of blood-brain barrier (BBB)-permeable, isoform-selective TYK2/JAK1 inhibitors. The aim is to generate candidates suitable for preclinical development in neuroinflammatory indications, such as multiple sclerosis and Parkinson’s disease.

Phosphorylation of the protein Tau is a key post-translational feature in tauopathies like Alzheimer’s disease (AD), which leads to microtubule dysfunction and Tau accumulation. Recent findings have suggested the blockade of the adenosine A2A receptor as an approach that improves the outcome in amyloid and Tau models.

Ischemic stroke triggers a strong neuroinflammatory response, with microglial activation and neutrophil infiltration contributing to blood-brain barrier disruption and worsening neuronal damage.