title: Alzheimer biomarkers and clinical Alzheimer disease were not associated with increased cerebrovascular disease in a memory clinic population.
abstract: 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.
authors.forename: Petra E
authors.initials: PE
authors.lastname: Spies
authors.forename: Marcel M
authors.initials: MM
authors.lastname: Verbeek
authors.forename: Magnus J C
authors.initials: MJ
authors.lastname: Sjogren
authors.forename: Frank-Erik
authors.initials: FE
authors.lastname: de Leeuw
authors.affiliation: Radboud university Medical Center, 925, Dept. Geriatric Medicine, P.O.Box 9101, 6500 HB Nijmegen, The Netherlands. Jurgen.Claassen@radboudumc.nl.
authors.forename: Jurgen A H R
authors.initials: JA
authors.lastname: Claassen
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid* / Q000235:genetics / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid*; D053327:Apolipoprotein E4 / Q000235:genetics*; D015415:Biomarkers / Q000134:cerebrospinal fluid; D001921:Brain / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000134:cerebrospinal fluid* / Q000235:genetics / Q000473:pathology; D005260:Female; D006801:Humans; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008569:Memory Disorders / Q000134:cerebrospinal fluid / Q000235:genetics / Q000473:pathology; D010446:Peptide Fragments / Q000134:cerebrospinal fluid*; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D016229:Amyloid beta-Peptides; D053327:Apolipoprotein E4; D015415:Biomarkers; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42)