Literature DB >> 14751769

Neuronal localization of C1q in preclinical Alzheimer's disease.

Maria I Fonseca1, Claudia H Kawas, Juan C Troncoso, Andrea J Tenner.   

Abstract

Complement has been postulated to contribute to inflammatory reactions associated with the neuropathology of Alzheimer's disease (AD). C1q, an initial component of the complement cascade, is associated with neuritic plaques and with neurons in the hippocampus of AD brain. Here, we report the presence of C1q in a cognitively intact subject, previously identified as preclinical AD. We compared in detail brain tissue of this preclinical case with a genetically related late-onset AD case. In the AD brain, C1q was typically associated with fibrillar Abeta plaques in frontal cortex and with plaques and neurons in the hippocampus. In the preclinical subject, C1q was abundantly present but it was cell-associated only, being primarily colocalized with neurons in both frontal cortex and hippocampus. However, no predominant cortical neuronal C1q localization was found in other preclinical cases or in Down's cases of different ages. Thus, it is possible that this neuronal-associated C1q reflects an early, but transient, response to injury that may modulate the progression of neurological dysfunction in AD.

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Year:  2004        PMID: 14751769     DOI: 10.1016/j.nbd.2003.09.004

Source DB:  PubMed          Journal:  Neurobiol Dis        ISSN: 0969-9961            Impact factor:   5.996


  28 in total

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2.  Highly specific inhibition of C1q globular-head binding to human IgG: a novel approach to control and regulate the classical complement pathway using an engineered single chain antibody variable fragment.

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Review 4.  Neuroimmune nexus of depression and dementia: Shared mechanisms and therapeutic targets.

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Review 5.  From development to dysfunction: microglia and the complement cascade in CNS homeostasis.

Authors:  Matthew K Zabel; Wolff M Kirsch
Journal:  Ageing Res Rev       Date:  2013-02-16       Impact factor: 10.895

Review 6.  Kainic acid-mediated excitotoxicity as a model for neurodegeneration.

Authors:  Qun Wang; Sue Yu; Agnes Simonyi; Grace Y Sun; Albert Y Sun
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Review 7.  Complement in the brain.

Authors:  Robert Veerhuis; Henrietta M Nielsen; Andrea J Tenner
Journal:  Mol Immunol       Date:  2011-05-04       Impact factor: 4.407

8.  C1q-induced LRP1B and GPR6 proteins expressed early in Alzheimer disease mouse models, are essential for the C1q-mediated protection against amyloid-β neurotoxicity.

Authors:  Marie E Benoit; Michael X Hernandez; Minhan L Dinh; Francisca Benavente; Osvaldo Vasquez; Andrea J Tenner
Journal:  J Biol Chem       Date:  2012-11-13       Impact factor: 5.157

9.  The role of the complement system and the activation fragment C5a in the central nervous system.

Authors:  Trent M Woodruff; Rahasson R Ager; Andrea J Tenner; Peter G Noakes; Stephen M Taylor
Journal:  Neuromolecular Med       Date:  2009-09-11       Impact factor: 3.843

10.  Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons.

Authors:  Christian S Lobsiger; Séverine Boillée; Don W Cleveland
Journal:  Proc Natl Acad Sci U S A       Date:  2007-04-26       Impact factor: 11.205

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