Multiple sclerosis (MS) is a degenerative and inflammatory condition of the central nervous system (CNS) that impacts more than 2.5 million individuals globally. Interleukin-33 (IL-33) is an immunoregulatory cytokine that has shown a mild inhibitory effect on experimental autoimmune encephalomyelitis (EAE), which serves as a mouse model for MS. However, its clinical application is limited by unfavorable pharmacokinetics and associated toxicity.

A recent study published in the journal International Immunopharmacology presents compelling preclinical evidence that NIMA-associated kinase 7 (NEK7), a key regulator of inflammation, may play a pivotal role in the pathology of depression.

The switch will be flicked today to make the world’s largest dementia-related proteomics dataset freely available to researchers, at the same time as members of the consortium which compiled it publish the proteomics signatures of major neurodegenerative diseases that they uncovered in a first trawl of the data.

A team of researchers from the University of Castilla-La Mancha, Spain, further investigated the link between hippocampal G protein-activated inward rectifier potassium channel (GIRK) and Alzheimer’s disease pathology.

“Loss of synapses and dysfunctional synapses in a region-specific way is important in Alzheimer’s. It’s actually the strongest correlate of cognitive decline, far more so than plaques and tangles, which are the pathological hallmarks,” Soyon Hong told the audience at the XVII Meeting on Glial Cells in Health and Disease, which was held in Marseille last week.

FAST kinase domain-containing protein 5 (FASTKD5) is a mitochondrial protein that is needed for processing mRNA in the primary mitochondrial transcript. Several mutations have been found in other proteins involved in mitochondrial metabolism, but mutations in the FASTKD5 gene have not yet been reported.

Progenra Inc. reports that it has discovered a new class of small-molecule PINK1 activators that restore function in mutant forms of the PINK1 kinase, a key mitochondrial regulator whose dysfunction leads to familial or early-onset Parkinson’s disease (PD).

Qanatpharma AG (QP), Zuse Institute Berlin (ZIB), Enamine Ltd. and Proteros biostructures GmbH have announced the launch of a research collaboration to accelerate the discovery of novel therapeutics targeting cerebral perfusion deficits associated with subarachnoid hemorrhage (SAH).