TMDU-led Japanese research revealed a role for splicing proteins in the pathology of Alzheimer’s disease. Increased phosphorylation of the SRRM2 protein, seen in AD mouse models and human patients, was found to block its transport to the nucleus. This reduced levels of the PQBP1 protein, causing abnormal changes to the splicing of synapse genes and cognitive decline. These phenotypes were reversed by restoring PQBP1 function, suggesting a possible future treatment for AD.
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