Perivascular Spaces Are Associated With CSF Aβ in Cerebral Amyloid Angiopathy but Not in Deep Perforator Arteriopathy.
Level 4 - case-series / case-control
Retrospective cross-sectional comparative observational study
PubMed 41778320 · doi:10.1161/STROKEAHA.125.053794
What was done
Retrospective analysis of 186 patients with cerebral small vessel disease (CSVD), comprising 111 with probable cerebral amyloid angiopathy (CAA) and 75 with deep perforator arteriopathy (DPA). Centrum semiovale perivascular spaces (CSO PVS) were quantified on axial T2-weighted MRI scans. Associations between CSO PVS counts and cerebrospinal fluid (CSF) amyloid-beta (Aβ) biomarkers (Aβ 42/40 ratio and Aβ 40) were evaluated using Pearson correlations and multivariable linear regression adjusting for demographics and neuroimaging CSVD markers, including an interaction term for CSVD subtype.
What was found
CSO PVS counts were similar between patients with CAA and DPA. Across the overall cohort, higher CSO PVS counts occurred in patients who were generally younger, had lower white matter hyperintensity burden, higher basal ganglia PVS counts, and more frequent cortical superficial siderosis. A significant interaction was observed between CSVD subtype and CSF Aβ 42/40 ratio on CSO PVS burden (interaction term β = -0.27; P = 0.016), indicating that CSO PVS burden was associated with CSF Aβ 42/40 ratio in CAA but not in DPA after multivariable adjustment. CSF Aβ 40 showed no association with CSO PVS counts in any model.
Why it matters
This study provides in vivo clinical evidence that centrum semiovale perivascular space enlargement specifically reflects impaired Aβ clearance in cerebral amyloid angiopathy rather than a uniform process across all small vessel disease subtypes. It highlights that the diagnostic and mechanistic significance of perivascular spaces depends on the underlying vascular pathology.
Limits
The study is retrospective and cross-sectional, precluding causal or temporal inferences. Probable CAA diagnoses were clinical and radiological rather than pathologically proven. The abstract does not report baseline biomarker concentrations, subgroup-specific correlation coefficients, or confidence intervals.
Cited by
- context Small vessel disease is a common cause of stroke and develops independently of amyloid accumulation.