Inflammation is a significant component of Alzheimer’s disease (AD) pathology. Regulatory T cells (Tregs) play a neuroprotective role by modulating innate and adaptive immune reactions. The Alireza Faridar lab documented that Tregs immunomodulatory function is compromised in AD individuals, shifting the immune system toward pro-inflammatory status. However, dysfunctional Tregs might be a restorable therapeutic target. In a preclinical AD murine model, restoration and expansion of Tregs, modified astrocytes and microglial activities, suppressed neuroinflammation and alleviated AD pathology. This treatment strategy has now been translated into a phase 1/2a clinical trials in AD individuals.
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