5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Utility of perfusion PET measures to assess neuronal injury in Alzheimer's disease

      research-article
      a , b , , a , c , a , a , a , a , a , d , e , e , f , d , d , g , h , i , d , j , k , a , f , d , f , l , m , n , c ,   d , d , a , Dominantly Inherited Alzheimer Network
      Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring
      Elsevier
      Alzheimer's disease, Neuronal injury, Perfusion, FDG, PiB

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction

          18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) is commonly used to estimate neuronal injury in Alzheimer's disease (AD). Here, we evaluate the utility of dynamic PET measures of perfusion using 11C-Pittsburgh compound B (PiB) to estimate neuronal injury in comparison to FDG PET.

          Methods

          FDG, early frames of PiB images, and relative PiB delivery rate constants (PiB-R1) were obtained from 110 participants from the Dominantly Inherited Alzheimer Network. Voxelwise, regional cross-sectional, and longitudinal analyses were done to evaluate the correlation between images and estimate the relationship of the imaging biomarkers with estimated time to disease progression based on family history.

          Results

          Metabolism and perfusion images were spatially correlated. Regional PiB-R1 values and FDG, but not early frames of PiB images, significantly decreased in the mutation carriers with estimated year to onset and with increasing dementia severity.

          Discussion

          Hypometabolism estimated by PiB-R1 may provide a measure of brain perfusion without increasing radiation exposure.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: not found
          • Article: not found

          An approximate distribution of estimates of variance components.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Imaging beta-amyloid burden in aging and dementia.

            To compare brain beta-amyloid (Abeta) burden measured with [(11)C]Pittsburgh Compound B (PIB) PET in normal aging, Alzheimer disease (AD), and other dementias. Thirty-three subjects with dementia (17 AD, 10 dementia with Lewy bodies [DLB], 6 frontotemporal dementia [FTD]), 9 subjects with mild cognitive impairment (MCI), and 27 age-matched healthy control subjects (HCs) were studied. Abeta burden was quantified using PIB distribution volume ratio. Cortical PIB binding was markedly elevated in every AD subject regardless of disease severity, generally lower and more variable in DLB, and absent in FTD, whereas subjects with MCI presented either an "AD-like" (60%) or normal pattern. Binding was greatest in the precuneus/posterior cingulate, frontal cortex, and caudate nuclei, followed by lateral temporal and parietal cortex. Six HCs (22%) showed cortical uptake despite normal neuropsychological scores. PIB binding did not correlate with dementia severity in AD or DLB but was higher in subjects with an APOE-epsilon4 allele. In DLB, binding correlated inversely with the interval from onset of cognitive impairment to diagnosis. Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. Noninvasive longitudinal studies to better understand the role of amyloid deposition in the course of neurodegeneration and to determine if Abeta deposition in nondemented subjects is preclinical AD are now feasible. Our findings also suggest that Abeta may influence the development of dementia with Lewy bodies, and therefore strategies to reduce Abeta may benefit this condition.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Regional aerobic glycolysis in the human brain.

              Aerobic glycolysis is defined as glucose utilization in excess of that used for oxidative phosphorylation despite sufficient oxygen to completely metabolize glucose to carbon dioxide and water. Aerobic glycolysis is present in the normal human brain at rest and increases locally during increased neuronal activity; yet its many biological functions have received scant attention because of a prevailing energy-centric focus on the role of glucose as substrate for oxidative phosphorylation. As an initial step in redressing this neglect, we measured the regional distribution of aerobic glycolysis with positron emission tomography in 33 neurologically normal young adults at rest. We show that the distribution of aerobic glycolysis in the brain is differentially present in previously well-described functional areas. In particular, aerobic glycolysis is significantly elevated in medial and lateral parietal and prefrontal cortices. In contrast, the cerebellum and medial temporal lobes have levels of aerobic glycolysis significantly below the brain mean. The levels of aerobic glycolysis are not strictly related to the levels of brain energy metabolism. For example, sensory cortices exhibit high metabolic rates for glucose and oxygen consumption but low rates of aerobic glycolysis. These striking regional variations in aerobic glycolysis in the normal human brain provide an opportunity to explore how brain systems differentially use the diverse cell biology of glucose in support of their functional specializations in health and disease.
                Bookmark

                Author and article information

                Contributors
                Journal
                Alzheimers Dement (Amst)
                Alzheimers Dement (Amst)
                Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring
                Elsevier
                2352-8729
                27 September 2018
                2018
                27 September 2018
                : 10
                : 669-677
                Affiliations
                [a ]Mallinckrodt Institute of Radiology, Washington University School of Medicine, Saint Louis, MO, USA
                [b ]Banner Alzheimer's Institute, Phoenix, AZ, USA
                [c ]Division of Biostatistics, Washington University School of Medicine, Saint Louis, MO, USA
                [d ]Department of Neurology, Washington University School of Medicine, Saint Louis, MO, USA
                [e ]Dementia Research Centre, UCL Institute of Neurology, London, UK
                [f ]Department of Neurology, Columbia University Medical Center, New York, NY, USA
                [g ]Department of Psychiatry, Washington University School of Medicine, Saint Louis, MO, USA
                [h ]Neuroscience Department Laboratories, Mount Sinai School of Medicine, New York, NY, USA
                [i ]Department of Radiology, Mayo Clinic, Rochester, MN, USA
                [j ]Departments of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
                [k ]Department of Radiology, University of Michigan, Ann Arbor, MI, USA
                [l ]Memory and Aging Center, Department of Neurology, Keck School of Medicine at the University of Southern California, Los Angeles, CA, USA
                [m ]Center for Neuroimaging, Department of Radiology and Imaging Science, Indiana University School of Medicine, Indianapolis, IN, USA
                [n ]Laboratory of Neuroimaging, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
                Author notes
                []Corresponding author. Tel.: +(602) 839 4851; Fax: +(602) 839 3498. yi.su@ 123456bannerhealth.com
                Article
                S2352-8729(18)30064-2
                10.1016/j.dadm.2018.08.012
                6215983
                30417072
                4e448f52-3b38-4024-b4a4-617610e012d3
                © 2018 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Neuroimaging

                alzheimer's disease,neuronal injury,perfusion,fdg,pib
                alzheimer's disease, neuronal injury, perfusion, fdg, pib

                Comments

                Comment on this article