TY - JOUR
T1 - Forebrain-dominant deficit in cerebrovascular reactivity in Alzheimer's disease
AU - Yezhuvath, Uma S.
AU - Uh, Jinsoo
AU - Cheng, Yamei
AU - Martin-Cook, Kristin
AU - Weiner, Myron
AU - Diaz-Arrastia, Ramon
AU - van Osch, Matthias
AU - Lu, Hanzhang
N1 - Funding Information:
The authors are grateful to Drs. Charles White, Karen Rodrigue and Kristen Kennedy for helpful discussions. This work was supported by Alzheimer Association NIRG 05–14,056 , National Institutes of Health R01 MH084021 , R21 AG034318 , R01 AG033106 , P30 AG12300 , and American Heart Association.
PY - 2012/1
Y1 - 2012/1
N2 - 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.
AB - 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.
KW - Alzheimer's disease
KW - Cerebral blood flow
KW - Cerebrovascular reactivity
KW - Magnetic resonance imaging
KW - Vascular function
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U2 - 10.1016/j.neurobiolaging.2010.02.005
DO - 10.1016/j.neurobiolaging.2010.02.005
M3 - Article
C2 - 20359779
AN - SCOPUS:79954421774
SN - 0197-4580
VL - 33
SP - 75
EP - 82
JO - Neurobiology of Aging
JF - Neurobiology of Aging
IS - 1
ER -