Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's diseaseCitation formats

  • Authors:
  • Stephen F Carter
  • Konstantinos Chiotis
  • Agneta Nordberg
  • Elena Rodriguez-Vieitez

Standard

Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease. / Carter, Stephen F; Chiotis, Konstantinos; Nordberg, Agneta; Rodriguez-Vieitez, Elena.

In: European Journal of Nuclear Medicine and Molecular Imaging, Vol. 46, No. 2, 02.2019, p. 348-356.

Research output: Contribution to journalArticlepeer-review

Harvard

Carter, SF, Chiotis, K, Nordberg, A & Rodriguez-Vieitez, E 2019, 'Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease', European Journal of Nuclear Medicine and Molecular Imaging, vol. 46, no. 2, pp. 348-356. https://doi.org/10.1007/s00259-018-4217-7

APA

Carter, S. F., Chiotis, K., Nordberg, A., & Rodriguez-Vieitez, E. (2019). Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease. European Journal of Nuclear Medicine and Molecular Imaging, 46(2), 348-356. https://doi.org/10.1007/s00259-018-4217-7

Vancouver

Carter SF, Chiotis K, Nordberg A, Rodriguez-Vieitez E. Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease. European Journal of Nuclear Medicine and Molecular Imaging. 2019 Feb;46(2):348-356. https://doi.org/10.1007/s00259-018-4217-7

Author

Carter, Stephen F ; Chiotis, Konstantinos ; Nordberg, Agneta ; Rodriguez-Vieitez, Elena. / Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease. In: European Journal of Nuclear Medicine and Molecular Imaging. 2019 ; Vol. 46, No. 2. pp. 348-356.

Bibtex

@article{ce0af54132344345baaeb681d0b087e0,
title = "Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease",
abstract = "PURPOSE: The spatial resolution of 18F-fluorodeoxyglucose PET does not allow the specific cellular origin of its signal to be determined, but it is commonly accepted that transport and trapping of 18F-fluorodeoxyglucose reflects neuronal glucose metabolism. The main frameworks for the diagnosis of Alzheimer's disease suggest that hypometabolism measured with 18F-fluorodeoxyglucose PET is a biomarker of neuronal injury and neurodegeneration. There is preclinical evidence to suggest that astrocytes contribute, at least partially, to the in vivo 18F-fluorodeoxyglucose PET signal. However, due to a paucity of PET tracers for imaging astrocytic processes, the relationship between astrocyte function and glucose metabolism in human brain is not fully understood. The aim of this study was to investigate the longitudinal association between astrocyte function and glucose metabolism in Alzheimer's disease.METHODS: The current investigation combined longitudinal PET data from patients with autosomal dominant Alzheimer's disease, including data on astrocyte function (11C-deuterium-L-deprenyl binding) and glucose metabolism (18F-fluorodeoxyglucose uptake). Research participants included 7 presymptomatic and 4 symptomatic mutation carriers (age 44.9 ± 9.8 years and 58.0 ± 3.7 years, respectively) and 16 noncarriers (age 51.1 ± 14.2 years). Eight carriers and eight noncarriers underwent longitudinal follow-up PET imaging at an average of 2.8 ± 0.2 and 3.0 ± 0.5 years from baseline, respectively.RESULTS: Longitudinal decline in astrocyte function as measured using 11C-deuterium-L-deprenyl PET was significantly associated with progressive hypometabolism (18F-fluorodeoxyglucose uptake) in mutation carriers; no significant association was observed in noncarriers.CONCLUSION: The emerging data shift the accepted wisdom that decreases in cerebral metabolism measured with 18F-fluorodeoxyglucose solely reflect neuronal injury, and places astrocytes more centrally in the development of Alzheimer's disease.",
keywords = "Adult, Alzheimer Disease/diagnostic imaging, Astrocytes/pathology, Female, Fluorodeoxyglucose F18, Glucose/metabolism, Humans, Longitudinal Studies, Male, Middle Aged, Mutation, Positron-Emission Tomography",
author = "Carter, {Stephen F} and Konstantinos Chiotis and Agneta Nordberg and Elena Rodriguez-Vieitez",
year = "2019",
month = feb,
doi = "10.1007/s00259-018-4217-7",
language = "English",
volume = "46",
pages = "348--356",
journal = "European Journal of Nuclear Medicine",
issn = "0340-6997",
publisher = "Springer Nature",
number = "2",

}

RIS

TY - JOUR

T1 - Longitudinal association between astrocyte function and glucose metabolism in autosomal dominant Alzheimer's disease

AU - Carter, Stephen F

AU - Chiotis, Konstantinos

AU - Nordberg, Agneta

AU - Rodriguez-Vieitez, Elena

PY - 2019/2

Y1 - 2019/2

N2 - PURPOSE: The spatial resolution of 18F-fluorodeoxyglucose PET does not allow the specific cellular origin of its signal to be determined, but it is commonly accepted that transport and trapping of 18F-fluorodeoxyglucose reflects neuronal glucose metabolism. The main frameworks for the diagnosis of Alzheimer's disease suggest that hypometabolism measured with 18F-fluorodeoxyglucose PET is a biomarker of neuronal injury and neurodegeneration. There is preclinical evidence to suggest that astrocytes contribute, at least partially, to the in vivo 18F-fluorodeoxyglucose PET signal. However, due to a paucity of PET tracers for imaging astrocytic processes, the relationship between astrocyte function and glucose metabolism in human brain is not fully understood. The aim of this study was to investigate the longitudinal association between astrocyte function and glucose metabolism in Alzheimer's disease.METHODS: The current investigation combined longitudinal PET data from patients with autosomal dominant Alzheimer's disease, including data on astrocyte function (11C-deuterium-L-deprenyl binding) and glucose metabolism (18F-fluorodeoxyglucose uptake). Research participants included 7 presymptomatic and 4 symptomatic mutation carriers (age 44.9 ± 9.8 years and 58.0 ± 3.7 years, respectively) and 16 noncarriers (age 51.1 ± 14.2 years). Eight carriers and eight noncarriers underwent longitudinal follow-up PET imaging at an average of 2.8 ± 0.2 and 3.0 ± 0.5 years from baseline, respectively.RESULTS: Longitudinal decline in astrocyte function as measured using 11C-deuterium-L-deprenyl PET was significantly associated with progressive hypometabolism (18F-fluorodeoxyglucose uptake) in mutation carriers; no significant association was observed in noncarriers.CONCLUSION: The emerging data shift the accepted wisdom that decreases in cerebral metabolism measured with 18F-fluorodeoxyglucose solely reflect neuronal injury, and places astrocytes more centrally in the development of Alzheimer's disease.

AB - PURPOSE: The spatial resolution of 18F-fluorodeoxyglucose PET does not allow the specific cellular origin of its signal to be determined, but it is commonly accepted that transport and trapping of 18F-fluorodeoxyglucose reflects neuronal glucose metabolism. The main frameworks for the diagnosis of Alzheimer's disease suggest that hypometabolism measured with 18F-fluorodeoxyglucose PET is a biomarker of neuronal injury and neurodegeneration. There is preclinical evidence to suggest that astrocytes contribute, at least partially, to the in vivo 18F-fluorodeoxyglucose PET signal. However, due to a paucity of PET tracers for imaging astrocytic processes, the relationship between astrocyte function and glucose metabolism in human brain is not fully understood. The aim of this study was to investigate the longitudinal association between astrocyte function and glucose metabolism in Alzheimer's disease.METHODS: The current investigation combined longitudinal PET data from patients with autosomal dominant Alzheimer's disease, including data on astrocyte function (11C-deuterium-L-deprenyl binding) and glucose metabolism (18F-fluorodeoxyglucose uptake). Research participants included 7 presymptomatic and 4 symptomatic mutation carriers (age 44.9 ± 9.8 years and 58.0 ± 3.7 years, respectively) and 16 noncarriers (age 51.1 ± 14.2 years). Eight carriers and eight noncarriers underwent longitudinal follow-up PET imaging at an average of 2.8 ± 0.2 and 3.0 ± 0.5 years from baseline, respectively.RESULTS: Longitudinal decline in astrocyte function as measured using 11C-deuterium-L-deprenyl PET was significantly associated with progressive hypometabolism (18F-fluorodeoxyglucose uptake) in mutation carriers; no significant association was observed in noncarriers.CONCLUSION: The emerging data shift the accepted wisdom that decreases in cerebral metabolism measured with 18F-fluorodeoxyglucose solely reflect neuronal injury, and places astrocytes more centrally in the development of Alzheimer's disease.

KW - Adult

KW - Alzheimer Disease/diagnostic imaging

KW - Astrocytes/pathology

KW - Female

KW - Fluorodeoxyglucose F18

KW - Glucose/metabolism

KW - Humans

KW - Longitudinal Studies

KW - Male

KW - Middle Aged

KW - Mutation

KW - Positron-Emission Tomography

U2 - 10.1007/s00259-018-4217-7

DO - 10.1007/s00259-018-4217-7

M3 - Article

C2 - 30515545

VL - 46

SP - 348

EP - 356

JO - European Journal of Nuclear Medicine

JF - European Journal of Nuclear Medicine

SN - 0340-6997

IS - 2

ER -