This review demonstrated that ischemic brain injury induces chronic changes in blood-brain barrier in the gray and white matter. This insufficiency of blood-brain barrier may allow entry of uncellular blood components such as different fragments of amyloid precursor protein and cellular blood components like leukocytes and platelets into the brain parenchyma. These blood components may have chronic harmful effects on the ischemic neuronal cells, axons and myelin and can intensify and finish the neuropathology in ischemic brain parenchyma. Pathological accumulation of different toxic fragments of amyloid precursor protein in extracellular space and myelinated axons appears after ischemic blood-brain barrier injury and seem to be concomitant with, but independent of neuronal ischemic cytoplasmic injury. It seems that ischemic blood-brain barrier disturbances may play an important, both direct and indirect role in the pathogenesis of extra- and intracellular space in gray and white matter lesions following ischemic episode. This neuropathology appears to have similar character and distribution as in sporadic Alzheimers disease. This review presented chronic micro-blood-brain barrier openings in ischemic gray and white matter lesions that probably would act as seeds of future Alzheimer ’ s amyloid plaques.
Keywords: Blood-brain barrier, brain ischemia, horseradish peroxidase, platelets, leukocytes, gray and white matter lesions, β-amyloid peptide, leukoaraiosis, amyloid plaques, Alzheimer's disease
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