Microglial activation is linked to cognitive impairment following repetitive mild closed head injury, with significant alterations in immune cell recruitment (ref: Mallah doi.org/10.1038/s41392-025-02466-7/).
Therapeutic modulation of microglial functions, such as with Lecanemab, shows promise in reducing amyloid pathology in Alzheimer's disease (ref: Albertini doi.org/10.1038/s41593-025-02125-8/).
Genetic factors, including a trisomy 21-associated gene variant, may confer resilience against Alzheimer's disease by influencing microglial activity (ref: Jin doi.org/10.1038/s41593-025-02117-8/).
Microglia-derived nanovesicles can synchronize autophagy pathways, highlighting their role in cellular homeostasis and potential therapeutic applications (ref: Li doi.org/10.1038/s41392-025-02453-y/).
Differential selectivity of microglia and astrocytes in synaptic pruning may inform therapeutic strategies in neurodegenerative diseases (ref: Watson doi.org/10.1093/brain/).
Microglial responses to environmental changes are critical for neuroinflammatory processes and cognitive outcomes following brain injury (ref: Mallah doi.org/10.1038/s41392-025-02466-7/).
The TMEM106B gene variant is associated with altered microglial activation and cytokine responses in chronic traumatic encephalopathy (ref: Hartman doi.org/10.1007/s00401-025-02955-7/).
Microglia play a multifaceted role in injury response and repair, influencing both astrocytic behavior and neuronal health (ref: Ni doi.org/10.1038/s41467-025-65095-2/).