Scientists have figured out how to protect the brain from abnormal proteins: they cause dementia

The study, conducted by scientists from the National Institute of Quantum Science and Technology in Japan,

demonstrated the critical role played by a specific gene—the p62 gene—in the selective autophagy of tau oligomers.

Previous studies have shown that abnormalaccumulation of tau proteins can be selectively suppressed by autophagy pathways through the p62 receptor protein (which is a selective autophagy receptor protein). The ability of this protein to bind to ubiquitin helps in the identification of toxic protein aggregates (such as tau oligomers), which can then be degraded by cellular processes and organelles.

However, the novelty of this study wasin demonstrating the “neuroprotective” role of p62 in a living model. Scientists haven't done this before. They used mouse models of dementia. The p62 gene was deleted in one group of animals, so they did not express p62 receptor proteins.

The authors of the work studied the brains of miceusing immunostaining and comparative biochemical analysis. As a result, they found aggregates of neurotoxic tau protein in the hippocampus - a region of the brain associated with memory - and the brain stem - the center that coordinates breathing, heartbeat, blood pressure and other voluntary processes - in mice with p62 knockout (p62KO, p62 knockout ).

MRI scans showed that the mouse hippocampusp62KO degenerated (atrophied) and became inflamed. Post-mortem brain assessment revealed extensive neuronal loss in the hippocampus. Further immunofluorescence studies showed that abnormal aggregates of tau species could cause cytotoxicity leading to inflammation and neuronal cell death in p62 KO mice. Oligomeric tau, in particular, accumulated more in the brains of p62KO mice.

Overall, the results of this study prove thatthat by eliminating and therefore preventing the aggregation of oligomeric tau species in the brain, p62 plays a neuroprotective role in models of dementia, protecting the brain.

Tau proteins, which otherwise play an important rolein stabilizing and maintaining the internal organization of neurons in the brain, accumulate abnormally within neurons in conditions such as dementia and Alzheimer's disease. This accumulation of hyperphosphorylated tau proteins (or tau oligomers) causes the formation of neurofibrillary tangles and eventual neuronal cell death in the brains of people with dementia, contributing to the progressive neurodegenerative symptoms of the disease. Although tau proteins can be degraded through selective autophagy, the exact mechanism of how this occurs has remained a mystery.

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