Abstract
BackgroundBlood–brain barrier (BBB) disruption has been noted in animal models of Parkinson’s disease (PD) and forms the basis of the vascular hypothesis of neurodegeneration, yet clinical studies are lacking.ObjectiveTo determine alterations in BBB integrity in PD, with comparison to cerebrovascular disease.MethodsDynamic contrast enhanced magnetic resonance images were collected from 49 PD patients, 15 control subjects with cerebrovascular disease [control positive (CP)] and 31 healthy control subjects [control negative (CN)], with all groups matched for age. Quantitative maps of the contrast agent transfer coefficient across the BBB (Ktrans) and plasma volume (vp) were produced using Patlak analysis. Differences in Ktrans and vp were assessed with voxel-based analysis as well as in regions associated with PD pathophysiology. In addition, the volume of white matter lesions (WMLs) was obtained from T2-weighted fluid attenuation inversion recovery (FLAIR) images.ResultsHigher Ktrans, reflecting higher BBB leakage, was found in the PD group than in the CN group using voxel-based analysis; differences were most prominent in the posterior white matter regions. Region of interest analysis confirmed Ktrans to be significantly higher in PD than in CN, predominantly driven by differences in the substantia nigra, normal-appearing white matter, WML and the posterior cortex. WML volume was significantly higher in PD compared to CN. Ktrans values and WML volume were similar in PD and CP, suggesting a similar burden of cerebrovascular disease despite lower cardiovascular risk factors.ConclusionThese results show BBB disruption in PD.
Highlights
The blood–brain barrier (BBB) consists of highly specialised, metabolically active cells forming a selectively permeable, highly resistant barrier to diffusion of blood products (Pardridge, 2005)
Dynamic contrast enhanced magnetic resonance images were collected from 49 Parkinson’s disease (PD) patients, 15 control subjects with cerebrovascular disease [control positive (CP)] and 31 healthy control subjects [control negative (CN)], with all groups matched for age
Higher contrast agent endothelial transfer coefficient (Ktrans), reflecting higher Blood–brain barrier (BBB) leakage, was found in the PD group than in the CN group using voxel-based analysis; differences were most prominent in the posterior white matter regions
Summary
The blood–brain barrier (BBB) consists of highly specialised, metabolically active cells forming a selectively permeable, highly resistant barrier to diffusion of blood products (Pardridge, 2005). It is closely coupled with glial cells (i.e., pericytes, microglia, oligodendroglia, and astrocyte end-feet), all in close proximity to a neuron; collectively termed the neurovascular unit (Lo and Rosenberg, 2009; Alvarez et al, 2013). Blood–brain barrier (BBB) disruption has been noted in animal models of Parkinson’s disease (PD) and forms the basis of the vascular hypothesis of neurodegeneration, yet clinical studies are lacking
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