Affiliations: [a] Department of Neurology, University Hospital RWTH Aachen, Aachen, Germany
| [b] JARA-Institute Molecular Neuroscience and Neuroimaging, Forschungszentrum Jülich, Jülich, Germany and RWTH Aachen University, Aachen, Germany
Correspondence:
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Correspondence to: Ana Sofia Costa, PhD, MSc, Department of Neurology, University Hospital RWTH Aachen & JARA Institute of Molecular Neuroscience and Neuroimaging. Address: Department of Neurology, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany. Tel.: +49 241 80 35601; Fax: +49 241 80 3335601; E-mail: acosta@ukaachen.de.
Abstract: Background:The overlap between cerebral amyloid angiopathy (CAA) and Alzheimer’s disease (AD) is frequent and relevant for patients with cognitive impairment. Objective:To assess the role of the diagnosis of CAA on the phenotype of amyloid-β (Aβ) positive patients from a university-hospital memory clinic. Methods:Consecutive patients referred for suspected cognitive impairment, screened for Aβ pathological changes in cerebrospinal fluid (CSF), with available MRI and neuropsychological results were included. We determined the association between probable CAA and clinical, neuropsychological (at presentation and after a mean follow-up of 17 months in a sub-sample) and MRI (atrophy, white matter hyperintensities, perivascular spaces) characteristics. Results:Of 218 amyloid-positive patients, 8.3% fulfilled criteria for probable CAA. A multivariable logistic regression showed an independent association of probable CAA with lower Aβ1–42 (adjusted odds ratio [aOR] = 0.94, 95% confidence interval [95% CI] = 0.90–0.98, p = 0.003), and Aβ1–40 (aOR = 0.98, 95% CI=0.97–0.99 p = 0.017) levels in CSF, and presence of severe burden of enlarged perivascular spaces (EPVS) in the centrum semiovale (aOR = 3.67, 95% CI = 1.21–11.15, p = 0.022). Linear mixed-model analysis showed that both groups significantly deteriorated in global clinical severity, executive function and memory. Nevertheless, the presence of probable CAA did not differently affect the rate of cognitive decline. Conclusion:The presence of probable CAA in Aβ positive patients was associated with lower Aβ1–42 and Aβ1–40 CSF levels and increased centrum semiovale EPVS burden, but did not independently influence clinical phenotype nor the rate of cognitive decline within our follow-up time window.
