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,
Jurgen A.H.R Claassen.
Objective: 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 β42, amyloid β40
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 β42, amyloid β40 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.
Keywords: Amyloid beta-peptides, apolipoproteins E, brain infarction, cerebrospinal fluid, dementia, leukoencephalopathies.
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