Send to

Choose Destination
See comment in PubMed Commons below
Tohoku J Exp Med. 1994 Nov;174(3):295-303.

Inflammatory response in Alzheimer's disease.

Author information

Division of Neuropathology, Tokyo Institute of Psychiatry, Japan.


Microglia belong to the mononuclear phagocyte system. They represent the brain resident tissue macrophages and function as the scavenger cells in brain. In Alzheimer's disease (AD), microglia become activated. Reactive microglia aggregate around senile plaque beta-amyloid and neurofibrillary tangles. Heavy accumulation of these pathological debris in postmortem, however, indicates the failure or, at best, partial success of the removal. It is supposed that continued activation of microglia in these lesions elicits a persistent inflammatory response. In fact, activation fragments of the complement system have been detected in association with beta-amyloid deposits and extracellular ghost tangles. Thrombin, a central serine protease of the coagulation pathway, is also deposited in these pathological debris. Both complements and thrombin could augment the biochemical, synthetic and phagocytic capacities of microglia. Microglia, in turn, might play a major role for the activation of complement and coagulation systems in brain. The available evidence strongly suggests a significant similarity between the chronic inflammation and the tissue response in AD lesions, supporting a notion that the inflammatory process is a part of Alzheimer pathology.

[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for J-STAGE, Japan Science and Technology Information Aggregator, Electronic
    Loading ...
    Support Center