Related Experiment Video For Alzheimer’s disease
Updated: Nov 20, 2025

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
Published on: March 7, 2019
Cerebral Amyloid Angiopathy in Amyloid-Positive Patients from a Memory Clinic Cohort
Ana Sofia Costa1,2, João Pinho1, Domantė Kučikienė1
1Department of Neurology, University Hospital RWTH Aachen, Aachen, Germany.
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.
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