The accumulation of neurotoxic peptides, activation of microglia, and neuroinflammation are hallmarks of many neurodegenerative diseases, including Alzheimer’s disease (AD). As the resident macrophages of the brain, microglia play a crucial role in the innate immune response of the central nervous system and are critical for neuronal development and homeostatic maintenance. Recent genome-wide studies have identified TREM2 (triggering receptor expressed on myeloid cells 2) as a key genetic risk factor, essential for the transition of homeostatic microglia to disease-associated microglia. Loss of TREM2 function is associated with neurodegeneration, as this prevents microglial transition and affects chemotaxis, phagocytosis, cell survival, and lipid and energy metabolism. Additionally, biomarker studies have revealed that TREM2 may protect humans from AD, so increasing TREM2 activity and preventing its proteolytic cleavage may be a new therapeutic approach. Once microglia detect extracellular threats and transition to a disease-associated state, they can release inflammatory mediators and trigger activation of the NLRP3 inflammasome, leading to the beta-amyloid deposition classically found in AD. Neuroinflammation can impair the ability of microglia to clear debris and can contribute to neuronal degeneration. In this webinar, the speakers will discuss key microglial functions and regulatory mechanisms necessary to maintain overall brain health, while revealing potential therapeutic targets in the fight against neurodegeneration.
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