Key studies in CAA.
| Authors | Study objective | Setting/Participants | Results | Notes |
|---|---|---|---|---|
| Banerjee et al. [60] (2020) | To assess CSF biomarkers in patients with CAA | CAA (n = 10), AD (n = 20), controls (n = 10) | Reduced CSF Aβ40 and Aβ42 levels in CAA compared to AD and controls; tau levels were intermediate | Supports the role of CSF biomarkers in distinguishing CAA from AD |
| Charidimou et al. [30] (2022) | To validate Boston criteria v2.0 for diagnosing CAA using MRI-neuropathology correlation | Multicenter retrospective study; n = 159 in the deviation cohort, n = 59 in the temporal validation cohort, n = 123 in the geographical validation cohort | Boston criteria v2.0 improved diagnostic sensitivity (74%) and maintained specificity (95%) | Established updated, reliable criteria for in vivo CAA diagnosis |
| Charidimou et al. [77] (2018) | Meta-analysis of CSF biomarkers in CAA | Pooled data from multiple studies (n = 3 studies: n = 59 CAA cases, n = 94 healthy controls, n = 158 AD cases) | Decreased Aβ40 and Aβ42 in CAA; variable tau levels | Confirms CSF profile differs from AD; suggests heterogeneity |
| Charidimou et al. [41] (2017) | Evaluate the detection and clinical implications of cortical superficial siderosis (cSS) in CAA | Mixed cohort with CAA and related conditions | cSS is strongly associated with the risk of future ICH and TFNEs | cSS is a key imaging marker in the Boston criteria |
| Kargiotis et al. [49] (2018) | Review of cerebral microbleeds (CMBs): causes, imaging, and clinical relevance | Literature review | Lobar CMBs are prominent in CAA and detectable via SWI/T2* MRI | Useful for differentiating CAA from hypertensive arteriopathy |
| Muir et al. [44] (2024) | Compare plasma biomarker quantification methods for AD and CAA application | Analytical comparison of biomarker assays | Combining biomarkers (Aβ ratio, p-tau, neuroinflammation, demographic/clinical variables) has the potential to improve the differential diagnosis of AD and CAA | Several methodological issues were identified: suggest using neuropathological gold standard, control for disease stage, essay standardization; sex differences and longitudinal changes |
| Paniagua Bravo et al. [51] (2014) | Compare MRI techniques for WMH detection | Healthy and clinical populations (n = 40 randomly selected patients; n = 10 controls) | 3D-FLAIR is superior in detecting WMHs compared to other sequences | Informs optimal MRI protocols for identifying WMHs in CAA |
| Seifert et al. [78] (2025) | Overview of diagnosis and management of CAA-related inflammation (CAA-ri) | Review article | CAA-ri is an immune-mediated variant with distinct imaging and steroid-responsive features | Highlights need to differentiate CAA-ri from sporadic CAA |
| Sin et al. [62] (2025) | Comprehensive review of plasma biomarkers for CAA in the context of ARIA | Review, including prospective biomarker studies | Plasma GFAP, Aβ42, and t-tau may predict CAA and ARIA risk | Suggests risk prediction with the potential plasma biomarkers for CAA in future studies |
| Smith et al. [39] (2021) | Characterize TFNEs in CAA and their clinical outcomes | Observational study of CAA patients with TFNEs | TFNEs are predictive of subsequent ICH and cSS | TFNEs should raise suspicion for underlying CAA |
| Theodorou et al. [37] (2023) | Examine the link between cSS, TFNEs, and lobar hemorrhage in CAA | Case series of CAA patients | TFNEs and cSS often precede symptomatic lobar hemorrhage | Reinforces the importance of early MRI detection of cSS in risk stratification |
CAA: cerebral amyloid angiopathy; CSF: cerebrospinal fluid; AD: Alzheimer’s disease; Aβ: amyloid β; MRI: magnetic resonance imaging; ICH: intracerebral hemorrhage; TFNEs: transient focal neurological episodes; SWI: susceptibility-weighted imaging; p-tau: phosphorylated tau; WMH: white matter hyperintensity; FLAIR: fluid-attenuated inversion recovery; ARIA: amyloid-related imaging abnormalities; GFAP: glial fibrillary acidic protein; t-tau: total tau.