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 VTT-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.
Theranocure Co. Ltd. has prepared and tested new vanillic acid derivatives targeting the dopamine D1 receptor (D1R) reported to be useful for the treatment of neuroinflammation and Alzheimer’s disease.
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).
The FKBP5 gene encodes FKBP prolyl isomerase 5, a co-chaperone that modulates glucocorticoid signaling and that is expressed in T cells, neurons and in microglial cells in the central nervous system (CNS). The role of FKBP5 in the dysregulation of myeloid cells in the pathogenesis of multiple sclerosis was investigated in a murine model of experimental autoimmune encephalomyelitis.
Researchers from Nanjing Drum Tower Hospital reported findings from their evaluation of the role of NLR family CARD domain containing 5 (NLRC5) in post-stroke neuroinflammation. Immunofluorescence staining of mouse brains revealed that NLRC5 was mainly expressed in microglia.
Bioage Labs Inc. has nominated BGE-102 as a development candidate. The orally available, small-molecule NLRP3 inhibitor has high potency and high brain penetration.