Forebrain-dominant deficit in cerebrovascular reactivity in Alzheimer's disease

Uma S. Yezhuvath, Jinsoo Uh, Yamei Cheng, Kristin Martin-Cook, Myron Weiner, Ramon Diaz-Arrastia, Matthias van Osch, Hanzhang Lu

Research output: Contribution to journalArticlepeer-review

66 Scopus citations

Abstract

Epidemiologic evidence and postmortem studies of cerebral amyloid angiopathy suggest that vascular dysfunction may play an important role in the pathogenesis of Alzheimer's disease (AD). However, alterations in vascular function under in vivo conditions are poorly understood. In this study, we assessed cerebrovascular-reactivity (CVR) in AD patients and age-matched controls using CO 2-inhalation while simultaneously acquiring Blood-Oxygenation-Level-Dependent (BOLD) MR images. Compared with controls, AD patients had widespread reduction in CVR in the rostral brain including prefrontal, anterior cingulate, and insular cortex (p < 0.01). The deficits could not be explained by cardiovascular risk factors. The spatial distribution of the CVR deficits differed drastically from the regions of cerebral blood flow (CBF) deficits, which were found in temporal and parietal cortices. Individuals with greater CVR deficit tended to have a greater volume of leukoaraiosis as seen on FLAIR MRI (p = 0.004). Our data suggest that early AD subjects have evidence of significant forebrain vascular contractility deficits. The localization, while differing from CBF findings, appears to be spatially similar to PIB amyloid imaging findings.

Original languageEnglish (US)
Pages (from-to)75-82
Number of pages8
JournalNeurobiology of Aging
Volume33
Issue number1
DOIs
StatePublished - Jan 2012

Keywords

  • Alzheimer's disease
  • Cerebral blood flow
  • Cerebrovascular reactivity
  • Magnetic resonance imaging
  • Vascular function

ASJC Scopus subject areas

  • Neuroscience(all)
  • Aging
  • Clinical Neurology
  • Developmental Biology
  • Geriatrics and Gerontology

Fingerprint Dive into the research topics of 'Forebrain-dominant deficit in cerebrovascular reactivity in Alzheimer's disease'. Together they form a unique fingerprint.

Cite this