Micro blood brain barrier openings and cytotoxic fragments of amyloid precursor protein accumulation in white matter after ischemic brain injury in long-lived rats.
This abstract is by R. Pluta, M. Ulamak and S. Januszewski from the dept. of neurodegenerative disorders at the Polish Academy of Science in Warsaw.
Our study demonstrates that ischemia-reperfusion brain injury induces an increase in blood brain barrier permeability in the periventricular white matter. This chronic insufficiency of blood brain barrier may allow entry of neurotoxic fragments of amyloid precursor protein and other blood components such as platelets into the perineurovascular white matter tissue.
These components may have secondary and chronic harmful effects on the ischemic myelin and axons and can intensify the phagocytic activity of microglial cells. Pathological accumulation of toxic fragments of amyloid precursor proteinin myelinated axons and oligodendrocytes appears after ischemic blood brain barrier injury and seem to be concomitant with, but independent of neuronal injury. It seems that ischemia-reperfusion disturbances may play important roles, both directly and indirectly, in the pathogenesis of white matter lesions. This pathology appears to have distribution similar to that of sporadic Alzheimer’s disease. We noted micro blood brain barrier openings in ischemic white matter lesions that probably would act as seeds of future Alzheimer’s-type pathology.
This abstract is available from pubmed using the identifier 16671468. The full articlu is available in the May 2006 issue of Acta Neurochirurgica starting on page 267.