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In vivo mitochondrial and glycolytic impairments in patients with Alzheimer disease
Abstract
Objective In vivo glycolysis-related glucose metabolism and electron transport chain-related mitochondrial activity may be different regionally in the brains of patients with Alzheimer disease (AD). To test this hypothesis regarding AD pathophysiology, we measured the availability of mitochondrial complex-I (MC-I) with the novel PET probe [ 18 F]2-tert- butyl-4-chloro-5-2H- pyridazin-3-one ([ 18 F]BCPP-EF), which binds to MC-I, and compared [ 18 F]BCPP-EF uptake with 18 F-fluorodeoxyglucose ([ 18 F]FDG) uptake in the living AD brain. Methods First, the total distribution volume (V T ) of [ 18 F]BCPP-EF from 10 normal controls (NCs) was quantified using arterial blood samples and then tested to observe whether V T could substitute for the standard uptake value relative to the global count (SUVRg). Eighteen NCs and 14 different NCs underwent PET with [ 18 F]BCPP-EF or [ 18 F]FDG, respectively. Second, 32 patients with AD were scanned semiquantitatively with double PET tracers. Interparticipant and intraparticipant comparisons of the levels of MC-I activity ([ 18 F]BCPP-EF) and glucose metabolism ([ 18 F]FDG) were performed. Results The [ 18 F]BCPP-EF V T was positively correlated with the [ 18 F]BCPP-EF SUVRg, indicating that the use of the SUVRg was sufficient for semiquantitative evaluation. The [ 18 F]BCPP-EF SUVRg, but not the [ 18 F]FDG SUVRg, was significantly lower in the parahippocampus in patients with AD, highlighting the prominence of oxidative metabolic failure in t…
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“Mitochondrial and glycolytic impairments had already been linked to AD before [30].”
From APOE4 Increases Energy Metabolism in APOE-Isogenic iPSC-Derived Neurons (2024) · cites this paper as [30]
In the citing paper
“Longitudinal studies confirm that reductions in cerebral metabolic rate of glucose (CMRglu) worsen with disease progression and strongly correlate with cognitive decline [69].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [69]
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APOE4 Increases Energy Metabolism in APOE-Isogenic iPSC-Derived Neurons
Budny, V., Knöpfli, Y., Meier, D., Zürcher, K., Bodenmann, C., Peter, S. L., Müller, T., Tardy, M., Cortijo, C., & Tackenberg, C. (2024) · Cells · doi:10.3390/cells13141207 · Cited by 15
Metadata
- Authors
- Terada, T., Obi, T., Bunai, T., Matsudaira, T., Yoshikawa, E., Ando, I., Futatsubashi, M., Tsukada, H., & Ouchi, Y.
- Affiliations
- Hamamatsu University (JP)
- Venue
- Neurology
- Published
- 2020-04-14
- Volume
- 94
- Issue
- 15
- Pages
- e1592-e1604
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W3009651604
- Cited by
- 103
- References
- 10
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 14 · 2023: 12 · 2022: 22 · 2021: 19 · 2020: 11
- FWCI
- 11.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (20K07901, 16H06402, 17K09797, 16H06400, 20H03600, 16H06277)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- Alzheimer's disease, mitochondrial dysfunction, mitochondrial complex I, 18F-FDG, glucose metabolism, glycolysis, parahippocampal region, medial temporal cortex, early Alzheimer's disease, regional brain metabolism, PET radiotracer
- MeSH terms
- Aged, Alzheimer Disease, Brain, Female, Glycolysis, Humans, Male, Mitochondria, Pyridines, Radiopharmaceuticals, Fluorodeoxyglucose F18
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