Global brain hypoperfusion and oxygenation in amnestic mild cognitive impairment

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  • Jie Liu
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA
  • Yong‐Sheng Zhu
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA
  • Muhammad Ayaz Khan
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA
  • Estee Brunk
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA
  • Kristin Martin‐Cook
    Department of Neurology and Neurotherapeutics and the Alzheimer's Disease Center University of Texas Southwestern Medical Center Dallas TX USA
  • Myron F. Weiner
    Department of Neurology and Neurotherapeutics and the Alzheimer's Disease Center University of Texas Southwestern Medical Center Dallas TX USA
  • C. Munro Cullum
    Department of Neurology and Neurotherapeutics and the Alzheimer's Disease Center University of Texas Southwestern Medical Center Dallas TX USA
  • Hanzhang Lu
    Advanced Imaging Research Center University of Texas Southwestern Medical Center Dallas TX USA
  • Benjamin D. Levine
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA
  • Ramon Diaz‐Arrastia
    Center for Neuroscience and Regenerative Medicine Uniformed Services University of the Health Sciences Bethesda MD USA
  • Rong Zhang
    Institute for Exercise and Environmental Medicine Texas Health Presbyterian Hospital Dallas Dallas TX USA

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<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>To determine if global brain hypoperfusion and oxygen hypometabolism occur in patients with amnestic mild cognitive impairment (aMCI).</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Thirty‐two aMCI and 21 normal subjects participated. Total cerebral blood flow (TCBF), cerebral metabolic rate of oxygen (CMRO<jats:sub>2</jats:sub>), and brain tissue volume were measured using color‐coded duplex ultrasonography (CDUS), near‐infrared spectroscopy (NIRS), and MRI. TCBF was normalized by total brain tissue volume (TBV) for group comparisons (nTCBF). Cerebrovascular resistance (CVR) was calculated as mean arterial pressure divided by TCBF.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Reductions in nTCBF by 9%, CMRO<jats:sub>2</jats:sub> by 11%, and an increase in CVR by 13% were observed in aMCI relative to normal subjects. No group differences in TBV were observed. nTCBF was correlated with CMRO<jats:sub>2</jats:sub> in normal controls, but not in aMCI.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Global brain hypoperfusion, oxygen hypometabolism, and neurovascular decoupling observed in aMCI suggest that changes in cerebral hemodynamics occur early at a prodromal stage of Alzheimer's disease, which can be assessed using low‐cost and bedside‐available CDUS and NIRS technology.</jats:p></jats:sec>

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