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Topography and Determinants of Magnetic Resonance Imaging (MRI)-Visible Perivascular Spaces in a Large Memory Clinic Cohort.

Topography and Determinants of Magnetic Resonance Imaging (MRI)-Visible Perivascular Spaces in a Large Memory Clinic Cohort.
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Shams S, Martola J, Charidimou A, Larvie M, Granberg T, Shams M, Kristoffersen-Wiberg M, Wahlund LO,


Shams S, Martola J, Charidimou A, Larvie M, Granberg T, Shams M, Kristoffersen-Wiberg M, Wahlund LO, (click to view)

Shams S, Martola J, Charidimou A, Larvie M, Granberg T, Shams M, Kristoffersen-Wiberg M, Wahlund LO,

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Journal of the American Heart Association 2017 09 226(9) pii e006279
Abstract
BACKGROUND
Magnetic resonance imaging-visible perivascular spaces (PVS) are related to interstitial fluid clearance pathways (including amyloid-β) in the brain and are suggested to be a marker of cerebral small vessel disease. We investigated the role, topography, and possible implications of PVS in cognitive impairment.

METHODS AND RESULTS
A total of 1504 patients undergoing memory clinic investigation and an associated brain magnetic resonance imaging scan were included in this cross-sectional study. Magnetic resonance images were assessed for markers of small vessel disease. Additionally, 1039 patients had cerebrospinal fluid analysis of amyloid-β 42, total tau (T-tau), and phosphorylated tau (P-tau); 520 patients had apoE genotyping done. Results were analyzed with generalized linear models. A total of 289 (19%; 95% confidence interval, 17-21) had a high-grade PVS in the centrum semiovale (CSO) and 65 (4%; 95% confidence interval: 3%-5%) in the basal ganglia (BG). Centrum semiovale- and BG-PVS were both associated with high age (P<0.001), hypertension (P<0.001), probable cerebral amyloid angiopathy (P<0.05), moderate-to-severe white matter hyperintensities (P<0.001), cortical superficial siderosis (P<0.001), cerebral microbleeds (P<0.001), and PVS. centrum semiovale-PVS was separately associated with strictly lobar cerebral microbleeds (P=0.057). BG-PVS was associated with strictly deep cerebral microbleeds (P<0.001), lacunes (P<0.001), and vascular dementia (P=0.04). BG-PVS showed a tendency to be associated with high cerebrospinal fluid tau (B=0.002, P=0.04) in the whole cohort and in Alzheimer's disease (B=0.005; P=0.02). No other associations with cerebrospinal fluid or the apoE e4 allele was observed. CONCLUSIONS
Centrum semiovale-PVS and BG-PVS have different underlying etiology, being associated with cerebral amyloid angiopathy and hypertensive vasculopathy, respectively, although a significant overlap between these pathologies is likely to exist.

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