Protein quality control research is “almost exclusively focused on heat shock proteins, which are ubiquitously present” up and down the evolutionary chain, Xiaolu Yang told BioWorld. But “for more sophisticated organisms, which we humans like to think we are, it’s a little odd that we still use the system that bacteria started with…. It seems like we should have something more. The TRIM system,” he added, “fills that gap.”

TRIMs or tripartite motif proteins are a group of quality control proteins that are found only in animals. One of their functions is to add ubiquitin tags to proteins, marking them for transport to the proteasome system. TRIMs are part of the innate antiviral defense system. But in the July 27, 2023, issue of Science, Yang, who is a professor of cancer biology in the Perelman School of Medicine at the University of Pennsylvania, and his colleagues reported that TRIM11 interacts with tau protein in multiple ways that were beneficial in preventing tauopathies.

Arsenal Medical Inc. said its Neocast embolic material for neurovascular conditions was successfully used to treat its first patient. The patient was embolized as part of a first-in-human study to assess the safety and feasibility of Neocast for the embolization of brain tumors to more easily enable surgical removal.

The identification of new targets in diseases of the central nervous system (CNS) such as Alzheimer’s and Parkinson’s – conditions which continue to have significant unmet needs – has taken a small step forward as one company, Violet Therapeutics Inc., plans to put $10.6 million in seed funding toward building out a pipeline based on technologies that elucidate the way cells interact amongst one another.

Juvenile neuronal ceroid lipofuscinosis (JNCL) is an inherited neurodegenerative disease caused by mutations in the gene encoding CLN3 lysosomal protein. Contrary to late-infantile neuronal ceroid lipofuscinosis (LINCL), caused by mutations in the lysosomal protein tripeptidyl peptidase 1 (TPP1), no animal models or effective treatment exist for JNCL. Previous research characterized mouse models with either mutated Tpp1 or Cln3, but the phenotype of a double Cln3/Tpp1 mutant, as well as the function of CLN3 protein, remain unclear.

Researchers from Arizona State University presented preclinical data for the novel dual specificity tyrosine phosphorylation kinase 1a (DYRK1a) inhibitor DYR-533, being developed for the treatment of tauopathies, including Alzheimer’s disease (AD).