The neurotropic alphavirus group includes Eastern equine encephalitis virus (EEEV), Venezuelan equine encephalitis virus (VEEV) and Western equine encephalitis virus (WEEV). These viruses exhibit a strong tropism for the CNS, often resulting in encephalitis. In some cases, infection can progress to severe neurological disease, including coma or death.

In multiple sclerosis (MS), an alteration of neuronal metabolism caused by dysfunction of its proteasome, the cellular machinery responsible for recycling proteins, contributes to neurodegeneration in this inflammatory disease. This finding could be explored for the development of drugs that protect neurons from damage in MS and other neurodegenerative disorders.

Bioxodes SA is gearing up fundraising for a follow-up study to the newly released interim phase IIa results of its lead asset in preventing secondary damage after an intracerebral hemorrhagic stroke. Data from the first 16 patients in the phase IIa study show BIOX-101 hit its primary safety and secondary endpoints in an indication that has no approved treatment.

Researchers from Violet Therapeutics Inc. presented the discovery of VT-001, a novel EPHB3 inhibitor designed to target astrocyte-mediated disease mechanisms.

The survival and plasticity of neurons depends on the signaling of the nerve growth factors BDNF and NGF acting through TRK receptors, which is crucial in neurological disorders such as Alzheimer’s disease (AD). Alzecure Pharma’s ACD-856 is a positive allosteric modulator (PAM) of TRK receptors that is in phase I trials for AD, and has shown good safety, pharmacokinetics and target engagement in the central nervous system.

At the recently launched Alzheimer’s & Parkinson’s Diseases Conference held in Vienna, Lotte Bjerre Knudsen from Novo Nordisk A/S, who has extensive experience in glucagon-like peptide-1 (GLP-1) research, delivered a plenary lecture focused on the role of GLP-1 receptor agonists, such as semaglutide, in attenuating neuroinflammation and neurodegeneration.

Tyrosine kinase 2 (TYK2), expressed in astrocytes and microglia, is involved in the activation of pathways triggered by proinflammatory cytokines, such as IL-23, IL-12 and type I interferons (IFNs), within the central nervous system (CNS). Dysregulated activation of astrocytes and microglia may contribute to the neuroinflammation associated with progressive forms of multiple sclerosis (MS).