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Co‐activation of Selective Nicotinic Acetylcholine Receptor Subtypes Is Required for Neuroprotection against Alzheimer's Disease

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Dysfunctional microglia-targeted nanoscavenger synergistically accelerates Aβ clearance and inhibits inflammatory cascade

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Aβ antibodies target not only amyloid plaques but also distinct brain cells and vessels

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Small Molecule Decoy of Amyloid-β Aggregation Blocks Activation of Microglia-Like Cells

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Multiscale Approximations to Understand the Complex Role of Microglia in Alzheimer's Disease

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Anti-Aβ immunotherapy-mediated amyloid clearance attenuates microglial activation without inducing exhaustion at residual plaquesPreprint

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β-Amyloid as a new target to suppress tonic PTH hypersecretion in primary hyperparathyroidismPreprint

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A bibliometric analysis of the current research status and hotspots regarding Aducanumab treatment for Alzheimer's disease

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Additional file 1 of Human brain organoids containing microglia that have arisen innately adapt to a β-amyloid challenge better than those in which microglia are integrated by co-culture

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Anti‐amyloid nanobody‐Fc fusion protein drives potent amyloid clearance through microglial recruitment

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Anti-Aβ immunotherapy-mediated amyloid clearance attenuates microglial activation without inducing exhaustion at residual plaquesPreprint

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Neuropathological study of the effects of aducanumab anti-Aβ immunotherapy on patients with Alzheimer’s disease

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Early intervention anti-Aβ immunotherapy attenuates microglial activation without inducing exhaustion at residual plaques

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Four-dimensional microglia response to anti-Aβ treatment in APP/PS1xCX3CR1/GFP mice

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