Recent evidence suggests that
inflammation in the central nervous system plays an important role in the pathogenesis of
Alzheimer's disease. However, the identity of the inflammatory mediators,
cytokines, and
reactive oxygen species, that orchestrate cell death and plaque biogenesis in
Alzheimer's disease, have yet to be elucidated. We have identified a novel inflammatory mediator,
CAP37 (Cationic Antimicrobial
Protein Mi 37 kDa), that promotes mononuclear cell chemotaxis, adhesion of monocytes to endothelium, and release of
oxygen radicals from monocytes. In the present immunocytochemical study, we demonstrate the expression of
CAP37 in the cerebral microvasculature in
Alzheimer's disease.
CAP37 was not detected in brain vessels of normal controls or patients with other neuropathologic conditions such as Pick's, Parkinson's,
Binswanger's disease,
Progressive Supranuclear Palsy, and
Candida infection. Treatment of cerebral endothelial cultures with inflammatory mediators,
cytokines or
beta-amyloid results in the induction of
CAP37 expression. These in vitro data showing endothelial-CAP37 expression after
beta-amyloid treatment together with the previous demonstration that
CAP37 stimulates mononuclear cell migration and activation, suggest that
CAP37 could contribute to neuronal injury in
Alzheimer's disease.