Association of CSF β-Amyloid Biomarker and Imaging Markers in Cerebral Amyloid Angiopathy

Background and Objectives Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by β-amyloid deposition in cerebral vessel walls, leading to hemorrhagic and ischemic injuries. The Boston criteria 2.0 guide CAA diagnosis based on clinical and neuroimaging findings. Although imaging-based phenotypes have been well-defined, data on CSF biomarkers remain limited. Integrating CSF and imaging markers may improve understanding of CAA disease patterns. This study evaluates associations between CSF and neuroimaging biomarkers in CAA. Methods We retrospectively selected patients with CAA diagnosed according to the Boston criteria 2.0 with available brain MRI and CSF. The amount of cortical superficial siderosis (cSS), the number of cerebral microbleeds (CMBs), enlarged perivascular spaces (EPVSs), and the presence of cortical microinfarcts (CMI) was assessed on brain MRI. Clinical records provided cerebrovascular risk factors and histories of lobar hemorrhage, subarachnoid hemorrhage (SAH), and ischemic stroke. CSF levels of β-amyloid 42 (Aβ42), β-amyloid 40 (Aβ40), Aβ42/40 ratio, total tau, and phosphorylated tau were recorded. Results Between June 2021 and May 2024, 23 patients (mean age 72.1 ± 8.4 SD, 52.1% female) met the inclusion criteria. All had lobar CMB and EPVS, while 78.2% had cSS and 65.2% had CMI. Adjusted regression analysis showed that lower Aβ40 levels were significantly associated with cSS extent (B = −0.50, 95% CI −0.96 to −0.044; p = 0.033) and CMI count (B = −0.30, 95% CI −0.57 to −0.034; p = 0.029). A lower Aβ42/40 ratio correlated with EPVS burden in the centrum semiovale (B = −0.18, 95% CI −0.35 to −0.012; p = 0.037). CMI were significantly associated with SAH (B = 0.87, 95% CI 0.23 to 1.51; p = 0.009). A trend toward an association was observed between EPVS burden and lobar hemorrhage (B = −0.36, 95% CI −0.75 to 0.017; p = 0.060). Discussion Lower CSF Aβ40 levels were associated with cSS and CMI, while a lower Aβ42/40 ratio correlated with EPVS burden. However, the small sample size and the lack of a control group represent a clear limitation, and the results can only have a preliminary and hypothesis-generating value. Further studies are needed to confirm these associations and explore their implications for disease progression and management.