Focusing on microglial mitochondria-lysosome crosstalk and neuroinflammation underlying depression: from molecular pathways to potential therapeutic interventions - PubMed
5 hours ago
- #depression
- #neuroinflammation
- #microglia
- Depression is a prevalent emotional disorder with significant global health impacts.
- Neuroinflammation is a key feature of depression, with microglia playing a crucial role in sensing and amplifying inflammation.
- Mitochondria-lysosome contact sites (MLCs) in microglia modulate metabolic states and inflammatory phenotypes.
- Disruption of MLCs leads to ROS accumulation, pro-inflammatory cytokine production, and neuroinflammatory cascades.
- Peripheral immune dysregulation, oxidative stress, and impaired autophagy contribute to neuroinflammation and depressive behaviors.
- Mitochondrial dysfunction and lysosomal pathology amplify inflammatory signaling in depression.
- Microglial MLCs abnormalities involve disrupted Ca²+ crosstalk, impaired autophagic flux, and redox imbalance.
- Emerging therapeutic strategies aim to restore MLC-regulated pathways for neuroinflammation-targeted antidepressant therapies.