Blood vessels and parkinsonism

Abstract

Blood vessels are the way for nutrients present outside the brain to gain access into the cerebral parenchyma. When neurons are diseased, for example by toxin exposure, reactive glial cells secrete local factors that induce microangiogenesis, probably as part of a spontaneous neuroprotective mechanism related to the increased metabolic demand. In Parkinson's disease (PD) and non human primate models of PD, nigral degeneration is associated with gliosis and microvascular proliferation. Interestingly, microangiogenesis also facilitates the entrance into the brain parenchyma of neurotoxins and harmful cytokine-releasing blood cells, both of which have been linked to neuronal cell death in PD. In the present review we discuss the potential implications of vascular-related phenomena with mechanisms of neuronal damage in PD.