The C5a complement activation peptide increases IL-1β and IL-6 release from amyloid-β primed human monocytes: implications for Alzheimer's disease

S O'Barr, NR Cooper - Journal of neuroimmunology, 2000 - Elsevier
Alzheimer's disease (AD) brains contain large numbers of amyloid-β peptide (Aβ) deposits
associated with activated microglia, astrocytes and dystrophic neurites. Activated …

Focal inflammation in the brain: role in Alzheimer's disease

NR Cooper, BM Bradt, S O'Barr, JX Yu - Immunologic Research, 2000 - Springer
We hypothesize that amyloid (Aβ) peptide-containing neuritic plaques in the brains of
patients with Alzheimer's disease represent chronic inflammatory foci mediated by the …

IL-4, IL-10 and IL-13 modulate Aβ (1–42)-induced cytokine and chemokine production in primary murine microglia and a human monocyte cell line

AM Szczepanik, S Funes, W Petko… - Journal of …, 2001 - Elsevier
A hallmark of the immunopathology associated with Alzheimer's disease (AD) is the
presence of activated microglia surrounding senile plaque deposits of β-amyloid (Aβ) …

Neuroglial-mediated immunoinflammatory responses in Alzheimer's disease: complement activation and therapeutic approaches

S Chen, RCA Frederickson, KR Brunden - Neurobiology of aging, 1996 - Elsevier
Increasing evidence points to Aβ-containing senile plaques as primary etiological agents in
Alzheimer's disease (AD). The mechanism by which these deposits cause neurotoxicity is …

Microglial C5aR (CD88) expression correlates with amyloid‐β deposition in murine models of Alzheimer's disease

RR Ager, MI Fonseca, SH Chu… - Journal of …, 2010 - Wiley Online Library
J. Neurochem.(2010) 113, 389–401. Abstract Alzheimer's disease (AD), a progressive
neurodegenerative disease characterized by the accumulation of amyloid‐β protein and …

Complement C1q expression induced by Aβ in rat hippocampal organotypic slice cultures

R Fan, AJ Tenner - Experimental neurology, 2004 - Elsevier
Amyloid β peptide (Aβ) is a major component of senile plaques, one of the principle
pathological features in Alzheimer's disease (AD) brains. Fibrillar Aβ has been shown to …

Complement component C1q modulates the phagocytosis of Aβ by microglia

SD Webster, AJ Yang, L Margol… - Experimental …, 2000 - Elsevier
Recent studies showing that microglia internalize the amyloid β-peptide (Aβ) suggest that
these cells have the potential for clearing Aβ deposits in Alzheimer's disease, and …

Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease

MI Fonseca, RR Ager, SH Chu, O Yazan… - The Journal of …, 2009 - journals.aai.org
Alzheimer's disease (AD) is an age-related dementia, characterized by amyloid plaques,
neurofibrillary tangles, neuroinflammation, and neuronal loss in the brain. Components of …

Cytokines associated with amyloid plaques in Alzheimer's disease brain stimulate human glial and neuronal cell cultures to secrete early complement proteins, but not …

R Veerhuis, I Janssen, CJA De Groot… - Experimental …, 1999 - Elsevier
Complement activation products C1q, C4c/d, and C3c/d in amyloid plaques in Alzheimer's
disease probably result from direct binding and activation of C1 by amyloid β peptides. RT …

Astrocyte-microglia cross talk through complement activation modulates amyloid pathology in mouse models of Alzheimer's disease

H Lian, A Litvinchuk, ACA Chiang… - Journal of …, 2016 - Soc Neuroscience
Increasing evidence supports a role of neuroinflammation in the pathogenesis of
Alzheimer's disease (AD). Previously, we identified a neuron–glia signaling pathway …