ArticlePeerJ2015
APOE genotype and age modifies the correlation between cognitive status and metabolites from hippocampus by a 2D (1)H-MRS in non-demented elders.
Article in PeerJ, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Mitochondrial dysfunction, oxidative stress, neuroinflammation, and metabolic alterations in the progression of Alzheimer's disease: A meta-analysis of in vivo magnetic resonance spectroscopy studies.Ageing research reviews · 2021Pooled it
- Article
- Understanding Proton Magnetic Resonance Spectroscopy Neurochemical Changes Using Alzheimer's Disease Biofluid, PET, Postmortem Pathology Biomarkers, and APOE Genotype.International journal of molecular sciences · 2024Review
- Article
- Effect of age and the APOE gene on metabolite concentrations in the posterior cingulate cortex.NeuroImage · 2017Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose. To examine the associations among age, Apolipoprotein E (APOE) genotype, metabolic changes in the hippocampus detected by 2D (1)H magnetic resonance spectroscopy (MRS), and neuropsychological measures of cognition in non-demented elders. Materials and Methods. We studied a cohort of 16 cognitively normal controls (CN) and 11 amnestic mild cognitive impairment (aMCI) patients between 66 and 88 years old who were genotyped for APOE genetic polymorphism. Measurements of 2D(1)H-MRS metabolites were obtained in the hippocampus region. Adjusting by age among all subjects, the association between metabolic changes and cognitive function was measured by Spearman partial rank-order correlation. The effect of APOE status was measured by separating the subjects into APOE genotype subgroups, including the APOEε4 carriers and APOEε4 non-carriers. Results. In contrast to the CN group matched with age, gender, and education, aMCI patients showed increased myo-inositol (mI)/Creatine (Cr) ratio only in the right hippocampus. No differences were noted on N-acetylaspartate (NAA)/Cr and mI/NAA from bilateral hippocampus, and so was mI/Cr ratio in left hippocampus between aMCI and CN. The mI/Cr ratio from the right hippocampus in non-demented elders was negatively correlated with Montreal Cognitive Assessment (MoCA) scores. Whether ε4 genotype or age was added as a covariate, none of the correlation effects remained significant. Additionally, adjusting for age and APOE genotype together, there was no significant correlation between them. Conclusion. Since the higher mI/Cr from the right hippocampus of the patients with aMCI than those from CN, the mI/Cr could be a more specific predictor of general cognitive function in aMCI patients. There is an association between higher mI/Cr in right hippocampus and worse cognitive function for the non-demented older adults, and the correlation could be modified by APOE status and age. That provided a window on objectively understanding the mechanism between the brain metabolites and the influence factors in non-demented elders.
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