A metabolic key to protecting the brain from tau
A new study reveals a protective role for astrocytic glycogen metabolism in tauopathies like Alzheimer’s disease. Researchers found that the glycogenolytic enzyme PYGM is upregulated in the brains of patients and mouse models. Crucially, astrocyte-specific knockout of PYGM worsened cognitive deficits and tau pathology in mice, while its overexpression—or direct supplementation with lactate, a key metabolic product—attenuated these disease-related phenotypes. The findings suggest that PYGM supports neuronal health by maintaining lactate-mediated metabolic coupling between astrocytes and neurons.
Why it might matter to you:
This work provides a concrete neurobiological mechanism—astrocyte-neuron metabolic coupling—that could be targeted to modify disease progression, a concept highly relevant to translational neuroscience. For a researcher focused on brain mechanisms in chronic conditions, it underscores the importance of non-neuronal cells and brain energetics as a frontier for therapeutic discovery. The study also offers a potential biomarker (glycogen metabolism) for assessing interventions in neurodegenerative disease.
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