Neuroinflammation has arisen as a key factor in the pathophysiology of Alzheimer’s disease (AD). Chronic immune activation in the brain leads to the release of pro-inflammatory cytokines and other inflammatory mediators that contribute to neuronal damage, thus impacting cognitive function during the progression of the disease. Transcriptomic and epigenomic analyses were performed to understand the epigenetic mechanisms behind the expression of inflammatory genes in AD brain.
The aberrant activation of NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a known crucial driver of neuroinflammation in Alzheimer’s disease (AD) and other related dementias. The inhibition of NLRP3 has shown benefits in preclinical models. Researchers from the University of Texas recently presented data regarding an NLRP3 inhibitor, AMS-17, for the treatment of AD and related dementias.
Vandria SA published phase I data on a potential new mechanism of action in treating Alzheimer’s disease, demonstrating its orally available and brain-penetrant mitochondria-boosting compound, VNA-318, engages its intended target.
Researchers from Novartis AG reported preclinical efficacy data on VHB-937, an agonist human monoclonal antibody targeting TREM2 in models of neuroinflammation.
Coya Therapeutics Inc. has released results of a study designed to evaluate the effects of COYA-303 (low dose IL-2 and a GLP-1 receptor agonist) in an established in vivo lipopolysaccharide mouse model of systemic and neuroinflammation. COYA-303 is an investigational proprietary combination for subcutaneous administration, under development for the treatment of diseases driven by chronic and sustained inflammation.
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.