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Abstract
Chronic mTORC1 hyperactivity is associated with mitochondrial dysfunction and neuroinflammation during aging.
- Aging leads to a decline in cellular homeostasis, increasing the risk of neurodegenerative diseases.
- mTORC1 plays a central role in regulating metabolism and integrating nutrient sensing with cellular growth.
- Overactivation of mTORC1, known as mTORopathy, contributes to the accumulation of toxic proteins like amyloid-beta and tau.
- Increased mTORC1 activity suppresses autophagy and glymphatic function, exacerbating neurodegeneration.
- Inhibition of mTORC1 through compounds like rapamycin may restore autophagic processes and reduce inflammation.
- Targeting mTORC1 could have potential therapeutic benefits for improving synaptic function and neurogenesis.
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