Alzheimers disease (AD) is a progressive neurodegenerative disorder distinguished not only by amyloid- (A) plaques and tau tangles but also by neuroinflammationprimarily orchestrated by microglia. These innate immune cells act as both protectors and contributors to pathology: initially aiding in A clearance and vascular maintenance, however, when chronically activated, driving persistent neuroinflammation, synaptic loss, and neuronal death. Importantly, the function of microglia is modulated by dynamic crosstalk with neuronsvia neurotransmitter signaling, cytokine exchanges, and direct contact. In particular, Shabestari et al demonstrated that microglia-deficient AD mice develop severe vascular and amyloid pathologies, which can be reversed by microglial transplantation, underscoring their protective role beyond plaque clearance. Disruptions in microglianeuron communication can critically influence AD progression and open avenues for targeted therapies modulating microglial behavior toward neuroprotection. This review summarizes nowadays findings into microglial biology in AD, focusing on neuron and microglia's interactions, molecular signaling, and strategies for accurately tuning microglial activity to maintain and protect cognitive function.
Jinxiang Na (Tue,) studied this question.