Complement component C3 and complement receptor type 3 contribute to the phagocytosis and clearance of fibrillar Aβ by microglia

Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

(2011) Dan Zhang et al.   Journal of Neuroinflammation

Complement receptor 3 (CD11b/CD18) is implicated in the elimination of β-amyloid peptides

(2010) Nada Choucair-Jaafar et al.   FUNDAMENTAL & CLINICAL PHARMACOLOGY

Inflammation and Microglia Actions in Alzheimer’s Disease

(2009) Colin K. Combs   Journal of Neuroimmune Pharmacology

Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain

(2009) Carol A. Colton   Journal of Neuroimmune Pharmacology

Formation and maintenance of Alzheimer's disease β-amyloid plaques in the absence of microglia

(2009) Stefan A Grathwohl et al.   NATURE NEUROSCIENCE

Immune Activation in Brain Aging and Neurodegeneration: Too Much or Too Little?

(2009) Kurt M. Lucin et al.   NEURON

Complement C3 Deficiency Leads to Accelerated Amyloid   Plaque Deposition and Neurodegeneration and Modulation of the Microglia/Macrophage Phenotype in Amyloid Precursor Protein Transgenic Mice

(2008) M. Maier et al.   JOURNAL OF NEUROSCIENCE

Dynamics of the Microglial/Amyloid Interaction Indicate a Role in Plaque Maintenance

(2008) T. Bolmont et al.   JOURNAL OF NEUROSCIENCE

Toll-Like Receptor 2 Acts as a Natural Innate Immune Receptor to Clear Amyloid  1-42 and Delay the Cognitive Decline in a Mouse Model of Alzheimer's Disease

(2008) K. L. Richard et al.   JOURNAL OF NEUROSCIENCE

Microglial Dysfunction and Defective  -Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice

(2008) S. E. Hickman et al.   JOURNAL OF NEUROSCIENCE

Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

(2008) Ganesh M Shankar et al.   NATURE MEDICINE