نقصان مغز جلویی غالب در واکنش پذیری عروق مغزی در بیماری آلزایمر

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 CO2-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.

. Conclusions Significant deficits in vessel reactivity are present in early AD patients. These deficits are most pronounced in rostral brain regions including prefrontal, anterior cingulate and insular cortices, and coincide with PIB rather than CBF findings, raising the possibility of an interaction between Aβ and vascular reactivity. Disclosure statement The authors declare that they have no conflict of interest, financial or otherwise, related to the present work.