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Complement Components and GFAP Immunoreactivity within Alzheimer and Pathologic Aged Cortex

  • Jia-Bao Pan
  • Chi-Ming Lee
  • Elliott J. Mufson
Part of the Advances in Behavioral Biology book series (ABBI, volume 44)

Abstract

The presence of amyloid plaques and neurofibrillary tangles are two prominent hallmarks in Alzheimer’s disease (AD) brains. Recent evidence suggests that reactive glial cells (astrocytes and microglia) and complement proteins play a pivotal role in the formation of the neuritic plaque pathology seen in AD (Dickson et al., 1988, 1993; McGeer et al., 1989; Eikelenboom et al., 1991; Ishii and Haga, 1992; Azmitia et al., 1992; Rogers et al., 1992; Wisniewski and Wegiel, 1992). Complement proteins collectively act as mediators of phagocytosis and cytolysis. These proteins mark tissues for phagocytosis (C1, C4, C2 and C3) and form channels in cell membranes (C5b-9, the membrane attack complex). Evidence for an involvement of complement activation in AD pathology includes: a) presence of focal immunoreactivity for Clq, C4d, Cab, C3c, C3d and C5b-9 on degenerating elements in AD brains, including amyloid plaques, tangles and dystrophic neuntes (McGeer et al., 1989; Eikelenboom et al., 1991; Rogers et al., 1992); b) higher level of Clq in the superior frontal cortex than in the cerebellum in AD brains, which correlates with more neuropathological changes in the frontal cortex (Lue and Rogers, 1992; Brachova et al., 1993); c) an increased expression of mRNA for ClgB, C3 and C4 in AD brains than in age-matched controls (Johnson et al., 1992; Walker and McGeer, 1992); and d) Aβ can bind to Clq and activate the classical complement cascade in an antibody independent manner (Rogers et al., 1992). Thus, the deposition of Aβ in amyloid plaques may trigger the activation of the classical complement pathway and contribute to the neuropathology in AD.

Keywords

Glial Fibrillary Acidic Protein Amyloid Plaque Complement Component Senile Plaque Neuritic Plaque 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1995

Authors and Affiliations

  • Jia-Bao Pan
    • 1
  • Chi-Ming Lee
    • 1
  • Elliott J. Mufson
    • 2
  1. 1.Neuroscience ResearchAbbott LaboratoriesAbbott ParkUSA
  2. 2.Department of Neurological SciencesAlzheimer’s Disease Center Rush Presbyterian St. Medical CenterChicagoUSA

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