Abstract
Monomeric-C-reactive protein (mCRP) is deposited in significant quantities within the brain parenchyma after stroke. Since we have recently identified a possible role of this protein in supporting neurodegeneration and aberrant vascular development, we identified a small group of post-mortem brain samples from individuals who had AD and on histological examination, evidence of tissue infarction/micro-infarction. Here we show that mCRP deposition is highest in those regions affected by stroke or vascular disruption, and that within those same areas, there is more interaction and co-localization between major classical proteins of neurodegeneration (beta-amyloid and tau. We hypothesise that vascular disruption and concomitant release of mCRP within the brain tissue could exacerbate ongoing neurological damage via stimulation of neuro-inflammation and from direct consequences of its action on both neuronal and vascular health.