2026 American Academy of Neurology Abstract Website

Hadrien Lalive¹, Federica Ribaldi², Augusto J Mendes², Chen Wang¹, Christian Chicherio³, Fabrizio Piazza⁴, Ilse Kern⁵, Cecilia Boccalini⁶, Elif Harput⁶, Valentina Garibotto⁷, Max Scheffler⁸, Karl Olof Lövblad⁹, Giovanni Frisoni², Aurélien Lathuilière¹⁰
¹Geneva Memory Center, Department of Rehabilitation and Geriatrics, Geneva University Hospitals and University of Geneva, Geneva, Switzerland, ²Geneva Memory Center, Department of Rehabilitation and Geriatrics, Geneva University Hospitals and University of Geneva, and Laboratory of Neuroimaging of Aging (LANVIE), University of Geneva, Geneva, Switzerland, ³Geneva Memory Center, Department of Rehabilitation and Geriatrics, Geneva University Hospitals and University of Geneva, and Center for Interdisciplinary Study of Gerontology and Vulnerability (CIGEV), University of Geneva, Geneva, Switzerland, ⁴CAA and AD Translational Research and Biomarkers Laboratory, iCAB International Network, School of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy, ⁵Diagnostic Department, Geneva University Hospitals, Geneva, Switzerland, ⁶Laboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), University of Geneva, Geneva, Switzerland, ⁷Laboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), University of Geneva, and Division of Nuclear Medicine and Molecular Imaging, Geneva University Hospitals, Geneva, Switzerland, ⁸Division of Radiology, Geneva University Hospitals, Geneva, Switzerland, ⁹Division of Neuroradiology, Geneva University Hospitals, Geneva, Switzerland, ¹⁰Geneva Memory Center, Department of Rehabilitation and Geriatrics, Geneva University Hospitals and University of Geneva, and Laboratory for Translational Research in Neurodegeneration, University of Geneva, Geneva, Switzerland

Objective:

To determine the frequency of cerebral amyloid angiopathy (CAA), defined by the Boston criteria v2.0, in biomarker-defined Alzheimer’s disease (AD) and to compare demographic, clinical, cognitive, and biomarker profiles between AD patients with probable and nonprobable CAA.

Background:

The Boston criteria are widely used in memory clinics to diagnose CAA, yet the prevalence and clinical significance of CAA among cognitively impaired patients with AD remain uncertain.

Design/Methods:

We retrospectively included 506 participants (mean age 74.0 ± 6.8 years; 58% female) with AD confirmed by amyloid-PET or cerebrospinal fluid (CSF) biomarkers from the Geneva University Hospitals Memory Center. MRI scans were evaluated by a neuroradiologist, independently reviewed by a trained image analyst, and confirmed by an experienced neurologist, the latter two blinded to clinical data. Participants were classified as AD-Probable CAA or AD-Nonprobable CAA (regrouping possible and no CAA) following the Boston criteria v2.0. Group comparisons used chi-square/Fisher tests for categorical variables and t-test/Mann-Whitney tests for continuous variables. Longitudinal cognitive decline was assessed with linear mixed-effects models. Associations between regional cerebral microbleed presence or burden and CSF biomarkers were analyzed using binary and ordinal logistic regression.

Results:

146 participants (29%) met criteria for probable CAA. AD-Probable CAA patients were older, more often received antiplatelet therapy, and had more prior ischemic strokes despite comparable vascular risk profiles. Baseline global and domain-specific cognition were similar between groups. Mini-Mental State Examination declined by 0.10 points/month with no group-level differences (p = .886). CSF Aβ42 levels were lower in AD-Probable CAA (p = .025) and associated with lobar CMBs, while cortical amyloid-PET uptake was higher (p < .05).

Conclusions:

Nearly one-third of biomarker-defined AD patients met Boston v2.0 criteria for probable CAA. CAA status was not associated with cognition or decline but reflected higher global amyloid burden, suggesting limited clinical utility of the Boston criteria in memory-clinic AD populations.