Inhibiting an important signaling pathway in brain-resident immune cells may calm brain inflammation and thereby slow the disease process in Alzheimer’s and some other neurodegenerative diseases, suggests a study by Weill Cornell Medicine investigators. The findings point to the possibility of new therapeutic strategies against neurodegenerative diseases, which are relatively common in older adults and so far have no effective, disease-modifying treatments. Brain inflammation, especially via the activation of immune cells in the brain called microglia, has long been noted as a common feature of neurodegenerative diseases. The spread of abnormal, thread-like aggregates—“tangles”—of a neuronal protein called tau is another frequent feature of these disorders. In the study, which appeared April 12, 2022 in Nature Communications, the researchers showed that the tau tangles help trigger the inflammatory activation of microglia, via a multifunctional signaling pathway called the NF-κB pathway. Inhibiting microglial NF-κB signaling in a tau-based Alzheimer’s mouse model largely pulled the immune cells out of their inflammatory state and reversed the animals’ learning and memory problems. The open-access article is titled “Microglial NF-κB Drives Tau Spreading and Toxicity in a Mouse Model of Tauopathy.”
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