Alzheimer Biomarkers and Clinical Alzheimer Disease were Not Associated with Increased Cerebrovascular Disease in a Memory Clinic Population
Petra E. Spies, Marcel M. Verbeek, Magnus J.C. Sjogren, Frank-Erik de Leeuw and Jurgen A.H.R ClaassenAffiliation:
Radboud university Medical Center, 925, Dept. Geriatric Medicine, P.O.Box 9101, 6500 HB Nijmegen, The Netherlands.
AbstractObjective: Preclinical and post-mortem studies suggest that Alzheimer disease (AD) causes cerebrovascular dysfunction, and therefore may enhance susceptibility to cerebrovascular disease (CVD). The objective of this study was to investigate this association in a memory clinic population. Methods: The AD biomarkers CSF amyloid β 42, amyloid β 40 and APOE- ε4 status have all been linked to increased CVD risk in AD, and therefore the first aim of this study was to analyze the association between these biomarkers and CVD. In 92 memory clinic patients the cross-sectional association between AD biomarkersand the severity of CVD was investigated with linear regression analysis. Additionally, we studied whether AD biomarkers modified the relation between vascular risk factors and CVD. CVD was assessed on MRI through a visual rating scale.Analyses were adjusted for age. The second aim of this study was to investigate the association between clinical AD and CVD, where ‘clinical AD’ was defined as follows: impairment in episodic memory, hippocampal atrophy and an aberrant concentration of cerebrospinal fluid (CSF) biomarkers. 47 of the 92 patients had AD. Results: No association between CSF amyloid β 42, amyloid β 40 or APOE- ε4 status and CVD severity was found, nor did these AD biomarkers modify the relation between vascular risk factors and CVD. Clinical AD was not associated with CVD severity (p=0.83). Patients with more vascular risk factors had more CVD, but this relationship was not convincingly modified by AD (p=0.06). Conclusions: In this memory clinic population, CVD in patients with AD was related to vascular risk factors and age, comparable to patients without AD. Therefore, in our study, the preclinical and post-mortem evidence that AD would predispose to CVD could not be translated clinically. Further work, including replication of this work in a different and larger sample, is warranted.
Amyloid beta-peptides, apolipoproteins E, brain infarction, cerebrospinal fluid, dementia, leukoencephalopathies.
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