ArticleStroke2026
Perivascular Spaces Are Associated With CSF Aβ in Cerebral Amyloid Angiopathy but Not in Deep Perforator Arteriopathy.
Article in Stroke, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCentrum semiovale perivascular spaces (CSO PVS) are common to different cerebral small vessel disease (CSVD) subtypes, yet their enlargement to the point of visibility on magnetic resonance imaging is thought to occur through distinct mechanisms. In cerebral amyloid angiopathy (CAA), CSO PVS are thought to reflect impaired perivascular Aβ (amyloid-β) drainage, whereas in deep perforator arteriopathy (DPA) they may result from microangiopathy-related arterial stiffening and altered fluid dynamics. The extent to which this can be confirmed in vivo remains unclear.
methodsWe retrospectively analyzed 186 patients with CSVD and cerebrospinal fluid (CSF) Aβ biomarkers (n=111 probable CAA, n=75 DPA). CSO PVS were counted on axial T2-weighted images. Associations between CSO PVS and CSF biomarkers were assessed via Pearson correlation and multivariable linear regression, including an interaction term between CSF Aβ and CSVD subtype, adjusted for demographics and neuroimaging markers of CSVD.
resultsPatients with higher CSO PVS counts were generally younger, had lower white matter hyperintensity burden, higher basal ganglia PVS counts, and were more frequently affected by cortical superficial siderosis. CSO PVS counts were similar in patients with CAA and DPA. The association between CSF Aβ
conclusionsOur findings strengthen the pathophysiological link between CSO PVS and Aβ pathology in CAA but not in DPA. These results extend previous histopathologic and neuroimaging work and underscore the need to interpret CSO PVS in the context of underlying CSVD subtype.
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