C4b-binding protein in Alzheimer's disease: Binding to Abeta(1-42) and to dead cells.

Leendert A Trouw, Henrietta Nielsen, Lennart Minthon, Elisabet Londos, Göran Landberg, Robert Veerhuis, Sabina Janciauskiene, Anna Blom

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

43 Citeringar (SciVal)

Sammanfattning

In the Alzheimer's disease (AD) brain, binding of Clq within the Cl complex, the initiating molecule of the classical complement pathway, to apoptotic cells, DNA and amyloid-beta (Abeta), the major constituent of senile plaques, can initiate complement activation. However, the extent of activation is determined by the balance between activation and inhibition. Fluid-phase complement inhibitor C4b-binding protein (C4BP) was immunohistochemically detected in Abeta plaques and on apoptotic cells in AD brain. In vitro, C4BP bound apoptotic and necrotic but not viable brain cells (astrocytes, neurons and oligodendrocytes) and limited complement activation on dead brain cells. C4BP also bound Abeta(1-42) peptide directly, via the C4BP alpha-chain, and limited the extent of complement activation by Abeta. C4BP levels in cerebrospinal fluid (CSF) of dementia patients and controls were low compared to levels in plasma and correlated with CSF levels of other inflammation-related factors. In conclusion, C4BP binds to dead brain cells and Abeta peptide in vitro, is present in CSF and possibly protects against excessive complement activation in AD brains.
Originalspråkengelska
Sidor (från-till)3649-3660
TidskriftMolecular Immunology
Volym45
DOI
StatusPublished - 2008

Ämnesklassifikation (UKÄ)

  • Immunologi inom det medicinska området

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