FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer’s disease
Open accessAbstract
Purpose We report the first clinicopathological series of longitudinal FDG-PET scans in post-mortem (PM) verified cognitively normal elderly (NL) followed to the onset of Alzheimer's-type dementia (DAT), and in patients with mild DAT with progressive cognitive deterioration.Methods Four NL subjects and three patients with mild DAT received longitudinal clinical, neuropsychological and dynamic FDG-PET examinations with arterial input functions. NL subjects were followed for 13 +/- 5 years, received FDG-PET examinations over 7 +/- 2 years, and autopsy 6 +/- 3 years after the last FDG-PET. Two NL declined to mild cognitive impairment (MCI), and two developed probable DAT before death. DAT patients were followed for 9 +/- 3 years, received FDG-PET examinations over 3 +/- 2 years, and autopsy 7 +/- 1 years after the last FDG-PET. Two DAT patients progressed to moderate-to-severe dementia and one developed vascular dementia.Results The two NL subjects who declined to DAT received a PM diagnosis of definite AD. Their FDG-PET scans indicated a progression of deficits in the cerebral metabolic rate for glucose (CMRglc) from the hippocampus to the parietotemporal and posterior cingulate cortices. One DAT patient showed AD with diffuse Lewy body disease (LBD) at PM, and her last in vivo PET was indicative of possible LBD for the presence of occipital as well as parietotemporal hypometabolism.Conclusion Progressive CMRglc reductions on FDG-PET occur years in advance of clinical DAT symptoms in patients with pathologically verified disease. The FDG-PET profiles in life were consistent with the PM diagnosis.
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Oxidative stress, mitochondrial dysfunction, and glucose hypometabolism have been well documented in MCI and AD brain.
“However, oxidative stress, mitochondrial dysfunction, and glucose hypometabolism have been well documented in MCI and AD brain [8,53,74,75,76].”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [76]
The Discussion (page not provided) reports reduced brain glucose metabolism in people progressing to MCI and Alzheimer’s dementia. The paper does not document the sentence’s other attributed findings, oxidative stress or mitochondrial dysfunction. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPatients with mild cognitive impairment and Alzheimer's disease exhibit deficits in brain energy metabolism years before symptom onset.
“Numerous studies show that patients with mild cognitive impairment (MCI) and AD exhibit deficits in brain energy metabolism years before disease symptom onset [8][9][10][11] .”
From APOE4-drives brain bioenergetic shifts independent of Alzheimer’s disease pathology (2026) · cites this paper as [11]
Regional reductions in brain glucose utilization occur with aging and to a greater extent in MCI and AD.
“Regional reductions in brain glucose utilization occur with aging and to a greater extent in MCI and AD [185-193].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [192]
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- Authors
- Mosconi, L., Mistur, R., Switalski, R., Tsui, W. H., Glodzik, L., Li, Y., Pirraglia, E., De Santi, S., Reisberg, B., Wisniewski, T., & de Leon, M. J.
- Affiliations
- New York University (US)
- Nathan Kline Institute for Psychiatric Research (US)
- Corresponding author
- Mosconi, Lisa
- Venue
- European Journal of Nuclear Medicine and Molecular Imaging
- Published
- 2009-01-14
- Volume
- 36
- Issue
- 5
- Pages
- 811-822
- ISSN
- 1619-7070 (ISSN-L)
- 1619-7089
- PMC
- PMC2774795
- OpenAlex
- W2043768383
- Cited by
- 487
- References
- 40
- Citations by year
- 2026: 23 · 2025: 29 · 2024: 27 · 2023: 23 · 2022: 36 · 2021: 29 · 2020: 25 · 2019: 38 · 2018: 22 · 2017: 30 · 2016: 24 · 2015: 27 · 2014: 34 · 2013: 30 · 2012: 30
- FWCI
- 18.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- European Journal of Nuclear Medicine and Molecular Imaging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG022374, AG03051, R01AG003051, R01AG022374, AG 12101, R01AG012101, P30AG008051, AG 08051, R01AG013616, AG 13616)
- National Center for Research Resources (M01RR0096, M01RR000096)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- Alzheimer's disease, FDG-PET, brain glucose metabolism, cerebral metabolic rate of glucose, mild cognitive impairment, dementia onset, postmortem neuropathology, posterior cingulate cortex, Lewy body disease, vascular dementia, arterial input function
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Autopsy, Brain, Cognition Disorders, Female, Glucose, Hippocampus, Humans, Male, Dementia, Vascular, Fluorodeoxyglucose F18, Lewy Body Disease, Positron-Emission Tomography
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