Evidence of blood–brain barrier disruption in Parkinson's disease (PD)

Desai, Brinda S.; Zhao, Chaohui; Ling, Zaodung; Lum, Hazel; Kim, K.S.; Schneider, Jacqueline; Carvey, Paul M.; Hendey, Bill

doi:10.1016/j.expneurol.2006.02.036

Cited by 1 publication

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“…There is accumulating evidence of microvascular changes and BBB dysfunction in PD patients and animal models of PD, with increased numbers of endothelial cells (Faucheux et al, 1999), and vascular growth in the substantia nigra pars compacta (Barcia et al, 2005;Carvey et al, 2005;Desai et al, 2005), possibly accompanied by increased BBB permeability Desai et al, 2005). In line with these findings, a recent positron emission tomography study has revealed a dysfunction of BBB efflux pumps in the midbrain of some PD patients with short disease duration (Kortekaas et al, 2005).…”

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confidence: 66%

Endothelial Proliferation and Increased Blood–Brain Barrier Permeability in the Basal Ganglia in a Rat Model of 3,4-Dihydroxyphenyl-l-Alanine-Induced Dyskinesia

Westin

Lindgren²,

Gardi³

et al. 2006

J. Neurosci.

114

132

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3,4-Dihydroxyphenyl-L-alanine (L-DOPA)-induced dyskinesia is associated with molecular and synaptic plasticity in the basal ganglia, but the occurrence of structural remodeling through cell genesis has not been explored. In this study, rats with 6-hydroxydopamine lesions received injections of the thymidine analog 5-bromo-2Ј-deoxyuridine (BrdU) concomitantly with L-DOPA for 2 weeks. A large number of BrdU-positive cells were found in the striatum and its output structures (globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata) in L-DOPA-treated rats that had developed dyskinesia. The vast majority (60 -80%) of the newborn cells stained positively for endothelial markers. This endothelial proliferation was associated with an upregulation of immature endothelial markers (nestin) and a downregulation of endothelial barrier antigen on blood vessel walls. In addition, dyskinetic rats exhibited a significant increase in total blood vessel length and a visible extravasation of serum albumin in the two structures in which endothelial proliferation was most pronounced (substantia nigra pars reticulata and entopeduncular nucleus). The present study provides the first evidence of angiogenesis and blood-brain barrier dysfunction in an experimental model of L-DOPA-induced dyskinesia. These microvascular changes are likely to affect the kinetics of L-DOPA entry into the brain, favoring the occurrence of motor complications.

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