Microglial Activation is Required for Aβ Clearance After Intracranial Injection of Lipopolysaccharide in APP Transgenic Mice

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Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse

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Microglial Phagocytosis of Fibrillar β-Amyloid through a β₁Integrin-Dependent Mechanism

2004 • 416 citations

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Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid β peptide in APPswe transgenic mice

2003 • 367 citations

Microglial Activation and β-Amyloid Deposit Reduction Caused by a Nitric Oxide-Releasing Nonsteroidal Anti-Inflammatory Drug in Amyloid Precursor Protein Plus Presenilin-1 Transgenic Mice

2002 • 344 citations

Scavenger receptors in neurobiology and neuropathology: Their role on microglia and other cells of the nervous system

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Bone-marrow-derived cells contribute to the recruitment of microglial cells in response to β-amyloid deposition in APP/PS1 double transgenic Alzheimer mice

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Intrahippocampal LPS injections reduce Aβ load in APP+PS1 transgenic mice

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Intracranially Administered Anti-Αβ Antibodies Reduce β-Amyloid Deposition by Mechanisms Both Independent of and Associated with Microglial Activation

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Glucocorticoids Play a Fundamental Role in Protecting the Brain during Innate Immune Response

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Microglial activation facilitates Aβ plaque removal following intracranial anti-Aβ antibody administration

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Dynamic Complexity of the Microglial Activation Response in Transgenic Models of Amyloid Deposition: Implications for Alzheimer Therapeutics

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Endogenous brain cytokine mRNA and inflammatory responses to lipopolysaccharide are elevated in the Tg2576 transgenic mouse model of Alzheimer’s disease

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Inflammation and primary demyelination induced by the intraspinal injection of lipopolysaccharide

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Time-dependent reduction in Aβ levels after intracranial LPS administration in APP transgenic mice

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Complement Component C1q Modulates the Phagocytosis of Aβ by Microglia

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Diverse microglial responses after intrahippocampal administration of lipopolysaccharide

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Neuroinflammation‐induced acceleration of amyloid deposition in the APP^V717F transgenic mouse

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Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease

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IL-10 and glucocorticoids inhibit Aβ(1–42)- and lipopolysaccharide-induced pro-inflammatory cytokine and chemokine induction in the central nervous system

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