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      Zero Echo Time 17O-MRI Reveals Decreased Cerebral Metabolic Rate of Oxygen Consumption in a Murine Model of Amyloidosis

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          Abstract

          The cerebral metabolic rate of oxygen consumption (CMRO 2) is a key metric to investigate the mechanisms involved in neurodegeneration in animal models and evaluate potential new therapies. CMRO 2 can be measured by direct 17O magnetic resonance imaging ( 17O-MRI) of H 2 17O signal changes during inhalation of 17O-labeled oxygen gas. In this study, we built a simple gas distribution system and used 3D zero echo time (ZTE-)MRI at 11.7 T to measure CMRO 2 in the APP swe/PS1 dE9 mouse model of amyloidosis. We found that CMRO 2 was significantly lower in the APP swe/PS1 dE9 brain than in wild-type at 12–14 months. We also estimated cerebral blood flow (CBF) from the post-inhalation washout curve and found no difference between groups. These results suggest that the lower CMRO 2 observed in APP swe/PS1 dE9 is likely due to metabolism impairment rather than to reduced blood flow. Analysis of the 17O-MRI data using different quantification models (linear and 3-phase model) showed that the choice of the model does not affect group comparison results. However, the simplified linear model significantly underestimated the absolute CMRO 2 values compared to a 3-phase model. This may become of importance when combining several metabolic fluxes measurements to study neuro-metabolic coupling.

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          Brain glucose metabolism in the early and specific diagnosis of Alzheimer's disease. FDG-PET studies in MCI and AD.

          Lisa Mosconi (2005)
          The demographics of aging suggest a great need for the early diagnosis of dementia and the development of preventive strategies. Neuropathology and structural MRI studies have pointed to the medial temporal lobe (MTL) as the brain region earliest affected in Alzheimer's disease (AD). MRI findings provide strong evidence that in mild cognitive impairments (MCI), AD-related volume losses can be reproducibly detected in the hippocampus, the entorhinal cortex (EC) and, to a lesser extent, the parahippocampal gyrus; they also indicate that lateral temporal lobe changes are becoming increasingly useful in predicting the transition to dementia. Fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) imaging has revealed glucose metabolic reductions in the parieto-temporal, frontal and posterior cingulate cortices to be the hallmark of AD. Overall, the pattern of cortical metabolic changes has been useful for the prediction of future AD as well as in distinguishing AD from other neurodegenerative diseases. FDG-PET on average achieves 90% sensitivity in identifying AD, although specificity in differentiating AD from other dementias is lower. Moreover, recent MRI-guided FDG-PET studies have shown that MTL hypometabolism is the most specific and sensitive measure for the identification of MCI, while the utility of cortical deficits is controversial. This review highlights cross-sectional, prediction and longitudinal FDG-PET studies and attempts to put into perspective the value of FDG-PET in diagnosing AD-like changes, particularly at an early stage, and in providing diagnostic specificity. The examination of MTL structures, which has so far been exclusive to MRI protocols, is then examined as a possible strategy to improve diagnostic specificity. All told, there is considerable promise that early and specific diagnosis is feasible through a combination of imaging modalities.
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            Amyloid deposition, hypometabolism, and longitudinal cognitive decline.

            Susan Landau, Mark Mintun, Abhinay D Joshi … (2012)
            Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. We examined associations between mean cortical florbetapir uptake, mean (18) F-fluorodeoxyglucose-positron emission tomography (FDG-PET) within a set of predefined regions, and Alzhiemer's Disease Assessment Scale (ADAS-cog) performance in 426 ADNI participants (126 normal, 162 early mild cognitive impairment [EMCI], 85 late MCI [LMCI], 53 Alzheimer disease [AD] patients). For a subset of these (76 normal, 81 LMCI) we determined whether florbetapir and FDG-PET were associated with retrospective decline in longitudinal ADAS-cog measurements. Twenty-nine percent of normal subjects, 43% of EMCI patients, 62% of LMCI patients, and 77% of AD patients were categorized as florbetapir positive. Florbetapir was negatively associated with concurrent FDG and ADAS-cog in both MCI groups. In longitudinal analyses, florbetapir-positive subjects in both normal and LMCI groups had greater ongoing ADAS-cog decline than those who were florbetapir negative. However, in normal subjects, florbetapir positivity was associated with greater ADAS-cog decline than FDG, whereas in LMCI, FDG positivity was associated with greater decline than florbetapir. Although both hypometabolism and β-amyloid (Aβ) deposition are detectable in normal subjects and all diagnostic groups, Aβ showed greater associations with cognitive decline in normal participants. In view of the minimal cognitive deterioration overall in this group, this suggests that amyloid deposition has an early and subclinical impact on cognition that precedes metabolic changes. At moderate and later stages of disease (LMCI/AD), hypometabolism becomes more pronounced and more closely linked to ongoing cognitive decline. Copyright © 2012 American Neurological Association.
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              Characterization of amyloid deposition in the APPswe/PS1dE9 mouse model of Alzheimer disease.

              Monica Garcia-Alloza, Elissa M Robbins, Sandy X Zhang-Nunes … (2006)
              Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy. We have characterized the natural history of beta-amyloid deposition in APPswe/PS1dE9 mice, a particularly aggressive transgenic mouse model generated with mutant transgenes for APP (APPswe: KM594/5NL) and PS1 (dE9: deletion of exon 9). Ex vivo histochemistry showed Abeta deposition by 4 months with a progressive increase in plaque number up to 12 months and a similar increase of Abeta levels. In vivo multiphoton microscopy at weekly intervals showed increasing beta-amyloid deposition as CAA and plaques. Although first appearing at an early age, CAA progressed at a significantly slower rate than in the Tg2576 mice. The consistent and early onset of beta-amyloid accumulation in the APPswe/PS1dE9 model confirms its utility for studies of biochemical and pathological mechanisms underlying beta-amyloid deposition, as well as exploring new therapeutic treatments.
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                Author and article information

                Contributors
                Andre F. Martins: Role: Academic Editor
                Myriam M. Chaumeil: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Metabolites
                Journal ID (iso-abbrev): Metabolites
                Journal ID (publisher-id): metabolites
                Title: Metabolites
                Publisher: MDPI
                ISSN (Electronic): 2218-1989
                Publication date (Electronic): 22 April 2021
                Publication date Collection: May 2021
                Volume: 11
                Issue: 5
                Electronic Location Identifier: 263
                Affiliations
                Laboratoire des Maladies Neurodégénératives, MIRCen, CNRS, CEA, Université Paris-Saclay, F-92260 Fontenay-aux-Roses, France; olivier.barret@ 123456cea.fr (O.B.); amelie.tourais@ 123456cea.fr (A.T.); jean-baptiste.perot@ 123456cea.fr (J.-B.P.); didier.thenadey@ 123456cea.fr (D.T.); fanny.petit@ 123456cea.fr (F.P.); Geraldine.Liot@ 123456cea.fr (G.L.); marie-claude.gaillard@ 123456cea.fr (M.-C.G.); julien.flament@ 123456cea.fr (J.F.); marc.dhenain@ 123456cea.fr (M.D.); julien.valette@ 123456cea.fr (J.V.)
                Author notes
                Author information
                https://orcid.org/0000-0003-4548-5630
                https://orcid.org/0000-0003-1187-6393
                https://orcid.org/0000-0002-6066-2909
                https://orcid.org/0000-0002-6412-3427
                Article
                Publisher ID: metabolites-11-00263
                DOI: 10.3390/metabo11050263
                PMC ID: 8145383
                PubMed ID: 33922384
                SO-VID: d3aa83fe-a56c-46a3-b91c-10ebf22efec7
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 21 March 2021
                Date accepted : 20 April 2021
                Categories
                Subject: Article

                Keywords: cerebral metabolic rate of oxygen,magnetic resonance imaging,oxygen-17,zero echo time,app/ps1,alzheimer’s disease,mouse
                Data availability:
                Keywords: cerebral metabolic rate of oxygen, magnetic resonance imaging, oxygen-17, zero echo time, app/ps1, alzheimer’s disease, mouse

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