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 …

A variety of inflammatory mediators including complement activation products, protease
inhibitors, and cytokines are colocalized with β-amyloid (Aβ) deposits in the Alzheimer's …

This review discusses key findings indicating potential roles of the complement (C)-system
in chronic inflammation in Alzheimer's disease (AD) brain. Although there is no means to …

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 …

We used reverse transcriptase-polymerase chain reaction and Western blotting techniques
to measure the levels of complement mRNAs and their protein products in Alzheimer's …

In Alzheimer's disease (AD) patients, the complement components Clq, C4 and C3 can be
detected in different types of β/A4 plaques, one of the hallmarks of AD. Contradictory …

We briefly describe the similarities and differences between a systemic and a local immune
reaction and review the evidence that the latter occurs in Alzheimer's disease (AD) brains …

Complement proteins are integral components of amyloid plaques and cerebral vascular
amyloid in Alzheimer brains. They can be found at the earliest stages of amyloid deposition …

It is now generally accepted that the lesions of Alzheimer disease (AD) are associated with a
host of inflammatory molecules, including complement proteins, as well as with many …

Complement inflammation is a major inflammatory mechanism whose function is to promote
the removal of microorganisms and the processing of immune complexes. Numerous …