Background Despite its identification as a key checkpoint regulator of microglial activation in
Alzheimer's disease, the overarching role of CX3CR1 signaling in modulating mechanisms …

Microglia, the primary immune effector cells in the brain, continually monitor the tissue
parenchyma for pathological alterations and become activated in Alzheimer's disease. Loss …

CX3CR1 is a chemokine receptor expressed on microglia that binds Fractalkine (CX3CL1)
and regulates microglial recruitment to sites of neuroinflammation. Full deletion of CX3CR1 …

Several Alzheimer's disease (AD) risk genes are specifically expressed by microglia within
the CNS. However, the mechanisms by which microglia regulate the pathological hallmarks …

Cx3cr1, the receptor for the chemokine Cx3cl1 (fractalkine), has been implicated in the
progression and severity of Alzheimer's disease-like pathology in mice, but the underlying …

In Alzheimer's disease (AD), amyloid-β (Aβ) deposits are frequently surrounded by activated
microglia but the precise role of these cells in disease progression remains unclear. The …

Aberrant microglial activation has been proposed to contribute to the cognitive decline in
Alzheimer disease (AD), but the underlying molecular mechanisms remain enigmatic …

CX3CR1, one of the highest expressed genes in microglia in mice and humans, is
implicated in numerous microglial functions. However, the molecular mechanisms …

The current mainstream doctrine in Alzheimer's disease (AD) is the amyloid cascade
hypothesis. According to this hypothesis, amyloid-β (Aβ) deposition is the main reason for …

Background Pharmacologic inhibition of C5aR1, a receptor for the complement activation
proinflammatory fragment, C5a, suppressed pathology and cognitive deficits in Alzheimer's …