ArticlebioRxiv : the preprint server for biology2025
Tau pathology reprograms glucose metabolism to support glutamatergic activity and excitatory imbalance.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Alzheimer's disease (AD) is not only characterized by amyloid-beta (Aβ) and tau pathology, but also by early and progressive disruptions in metabolism. Neuronal excitability is tightly coupled with metabolic demand, and aberrant excitatory activity - observed in AD patients and models - can drive changes in metabolism. While Aβ-related metabolic impairments are well-described, less is known about how tau pathology independently contributes to altered metabolic states and excitatory tone. Therefore, we explored how tau pathology impacted whole body and CNS metabolism in mouse models of tauopathy, including the P301S PS19 and Tau4RTg2652 mice. In both models, hyperphosphorylated tau prevents the age-related decline in whole-body metabolism by preserving glucose tolerance and mitigating shifts in fuel utilization (respiratory exchange ratio; RER), suggesting the mice are "glucose needy". Tau pathology also preserves diurnal rhythms in hippocampal interstitial fluid (ISF) glucose and lactate, likely due to increased neuronal activity during the active (dark) phase. Stable isotope-resolved metabolomics following
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