2011
DOI: 10.2174/156720511794604589
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Histological and Direct Evidence for the Role of Complement in the Neuroinflammation of AD

Abstract: In Alzheimers's disease (AD) a disturbed balance between synthesis and removal of Aβ leads to the formation of Aβ deposits and a reaction of the innate immune system. Little evidence exists for a contribution of the adaptive immune response in AD, as no signs of influx of blood borne cells or presence of immunoglobulins in Aβ deposits are apparent. Factors of the complement(C) system and pentraxins act as pattern recognition molecules and mediate uptake of Aβ by glial cells expressing C-receptors (Crec). These… Show more

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Cited by 77 publications
(60 citation statements)
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References 222 publications
(433 reference statements)
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“…Neuronal pentraxins (NPs), which have key roles in neuroinflammation (15), belong to a family of proteins that are homologous to immune system proteins, including C-reactive and acute phase proteins, and are believed to be involved in synaptic functions (16). The NPs, including NP1, NP2 and NP receptor (NPR) (17), are proteins that were initially identified due to their ability to bind to the snake poison taipoxin (18) and mediate its internalization, leading to cell death.…”
Section: Introductionmentioning
confidence: 99%
“…Neuronal pentraxins (NPs), which have key roles in neuroinflammation (15), belong to a family of proteins that are homologous to immune system proteins, including C-reactive and acute phase proteins, and are believed to be involved in synaptic functions (16). The NPs, including NP1, NP2 and NP receptor (NPR) (17), are proteins that were initially identified due to their ability to bind to the snake poison taipoxin (18) and mediate its internalization, leading to cell death.…”
Section: Introductionmentioning
confidence: 99%
“…Aβ1-42 is more prone to oligomerization and more readily forms the aggregates present in AD (Schroeter et al, 2003;Cai et al, 2001;Iwatsubo et al, 1994). Deposition of Aβ plaques in the brain is also associated with neuronal damage and activation of local astrocytes and microglia, resulting in localized inflammatory responses (Veerhuis, 2011;Eikelenboom and Stam, 1982;Eikelenboom et al, 1989;Eikelenboom and Veerhuis, 1996;Rosenberg, 2005). However, accumulation of Aβ plaques is not necessarily either a cause or a consequence of AD, as plaques can be found in the brains of cognitively healthy individuals (Walsh et al, 2000).…”
Section: Alzheimer Disease Pathology and Basic Science Animal Researchmentioning
confidence: 99%
“…Complement proteins associated with the 'classical' pathway [123], brain reactive antibodies [132], immunoglobulins [62,95], circulating immune complexes (CIC) in peripheral tissue and cerebral blood vessels [86], helper/inducer and cytotoxic/ suppressor T-cells [123], and abundant reactive microglia [123] have all been observed in AD. Complement system proteins may act as pattern recognition molecules mediating the uptake of Ab by glial cells which express complement receptors [195]. Significant alterations in the major histocompatibility locus (MHC) antigens have also been demonstrated [197] suggesting either increased resistance or susceptibility to an antigen in AD [50,88].…”
Section: Theories Based On Immunologymentioning
confidence: 99%