Correlations between apolipoprotein E ε4 gene dose and brain-imaging measurements of regional hypometabolism
Open accessAbstract
Patients with Alzheimer's disease (AD) have abnormally low positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex. Apolipoprotein E (APOE) ε4 gene dose (i.e., the number of ε4 alleles in a person's APOE genotype) is associated with a higher risk of AD and a younger age at dementia onset. We previously found that cognitively normal late-middle-aged APOE ε4 carriers have abnormally low CMRgl in the same brain regions as patients with probable Alzheimer's dementia. In a PET study of 160 cognitively normal subjects 47–68 years of age, including 36 ε4 homozygotes, 46 heterozygotes, and 78 ε4 noncarriers who were individually matched for their gender, age, and educational level, we now find that ε4 gene dose is correlated with lower CMRgl in each of these brain regions. This study raises the possibility of using PET as a quantitative presymptomatic endophenotype to help evaluate the individual and aggregate effects of putative genetic and nongenetic modifiers of AD risk.
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Both young and old APOE4 carriers display decreased glucose utilization, measured by FDG-PET, in brain regions similar to those seen with AD patients.
“early reports by Reiman and colleagues demonstrated that both young and old APOE4 carriers display decreased glucose utilization, as measured by fluorodeoxyglucose positron emission tomography (FDG-PET), in brain regions similar to those seen with AD patients16–18.”
From APOE4 is Associated with Differential Regional Vulnerability to Bioenergetic Deficits in Aged APOE Mice (2020) · cites this paper as [18]
The Results report lower FDG-PET measurements of glucose metabolism in APOE ε4 carriers in regions also implicated in Alzheimer’s dementia. The study examined cognitively normal people aged 47–68 (study summary and Methods; page unavailable), so it does not establish the claim for both young and old carriers. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPerturbed brain energy metabolism is one of the major changes that typically occurs in the preclinical Alzheimer's disease brain.
“One of the major changes that typically occurs in the preclinical AD brain is the perturbed brain energy metabolism.”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Reiman et al., 2005
The paper’s opening section and Results report reduced regional glucose metabolism in cognitively normal, late-middle-aged APOE ε4 carriers, consistent with a metabolic change before symptoms. But these participants were at increased risk of AD, not established to have preclinical AD; the Discussion says the study could not yet determine whether they would develop it. The paper therefore does not establish that this change typically occurs in the preclinical AD brain. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe brains of APOE4 carriers display decreased glucose utilization in numerous AD-relevant brain regions, as observed by FDG-PET.
“As shown in previous studies, the brains of APOE4 carriers display decreased glucose utilization in numerous AD-relevant brain regions, as observed by FDG-PET16–18.”
From APOE4 is Associated with Differential Regional Vulnerability to Bioenergetic Deficits in Aged APOE Mice (2020) · cites this paper as [18]
Cognitively normal individuals at risk for Alzheimer's disease, including ApoE4 carriers, show reduced cerebral metabolism of glucose.
“Cognitively normal individuals at risk for AD, including those carrying ApoE4, showed reduced cerebral metabolism of glucose (Reiman et al., 2004(Reiman et al., , 2005)).”
From Human ApoE Isoforms Differentially Modulate Brain Glucose and Ketone Body Metabolism: Implications for Alzheimer's Disease Risk Reduction and Early Intervention (2018) · cites this paper as Reiman et al., 2005
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Self-citation
- Authors
- Reiman, E. M., Chen, K., Alexander, G. E., Caselli, R. J., Bandy, D., Osborne, D., Saunders, A. M., & Hardy, J.
- Affiliations
- Mayo Clinic (US)
- National Institutes of Health (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2005-06-02
- Volume
- 102
- Issue
- 23
- Pages
- 8299-8302
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC1149416
- OpenAlex
- W1622703765
- Cited by
- 401
- References
- 4
- Citations by year
- 2026: 9 · 2025: 6 · 2024: 14 · 2023: 14 · 2022: 10 · 2021: 26 · 2020: 22 · 2019: 19 · 2018: 20 · 2017: 12 · 2016: 20 · 2015: 13 · 2014: 20 · 2013: 18 · 2012: 22
- FWCI
- 14.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute on Aging (AG-19610, P30AG019610)
- National Institute of Mental Health (MH57899, R01MH057899)
- 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
- APOE ε4, APOE genotype, gene dosage, Alzheimer's disease, brain glucose metabolism, precuneus, posterior cingulate cortex, temporoparietal cortex, frontal cortex, genetic risk factors, dementia risk
- MeSH terms
- Aged, Alleles, Alzheimer Disease, Apolipoproteins E, Brain, Female, Genotype, Glucose, Humans, Magnetic Resonance Imaging, Male, Metabolic Diseases, Middle Aged, Phenotype, Age of Onset, Gene Dosage, Positron-Emission Tomography, Apolipoprotein E4
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