Brain aerobic glycolysis and resilience in Alzheimer disease.

Autor:	Goyal MS; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110.; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108.; Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110., Blazey T; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110., Metcalf NV; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110., McAvoy MP; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110.; Program in Occupational Therapy, Washington University School of Medicine, St. Louis, MO 63108., Strain JF; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110., Rahmani M; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110., Durbin TJ; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110., Xiong C; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108., Benzinger TL; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110.; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108., Morris JC; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108., Raichle ME; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110.; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108.; Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110.; Department of Biomedical Engineering, Washington University School of Medicine, St. Louis, MO 63130.; Department of Psychology & Brain Science, Washington University School of Medicine, St. Louis, MO 63130., Vlassenko AG; Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO 63110.; Neuroimaging Labs Research Center, Washington University School of Medicine, St. Louis, MO 63110.; Knight Alzheimer Disease Research Center, Washington University School of Medicine, St. Louis, MO 63108.
Jazyk:	angličtina
Zdroj:	Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2023 Feb 14; Vol. 120 (7), pp. e2212256120. Date of Electronic Publication: 2023 Feb 06.
DOI:	10.1073/pnas.2212256120
Abstrakt:	The distribution of brain aerobic glycolysis (AG) in normal young adults correlates spatially with amyloid-beta (Aβ) deposition in individuals with symptomatic and preclinical Alzheimer disease (AD). Brain AG decreases with age, but the functional significance of this decrease with regard to the development of AD symptomatology is poorly understood. Using PET measurements of regional blood flow, oxygen consumption, and glucose utilization-from which we derive AG-we find that cognitive impairment is strongly associated with loss of the typical youthful pattern of AG. In contrast, amyloid positivity without cognitive impairment was associated with preservation of youthful brain AG, which was even higher than that seen in cognitively unimpaired, amyloid negative adults. Similar findings were not seen for blood flow nor oxygen consumption. Finally, in cognitively unimpaired adults, white matter hyperintensity burden was found to be specifically associated with decreased youthful brain AG. Our results suggest that AG may have a role in the resilience and/or response to early stages of amyloid pathology and that age-related white matter disease may impair this process.
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu