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Objective. To determine the regional effects of age and sex on the metabolic ratios obtained in the medial temporal lobe, the posteromedial region, and the frontal lobe at 1.5T single-voxel magnetic resonance spectroscopy. Material and methods. We used single-voxel magnetic resonance spectroscopy to study the areas of the brain most affected in neurodegenerative disease (the left frontal lobe, the left medial temporal lobe, and the posteromedial region) in 31 healthy subjects older than 55 years of age (group 1) and in 20 healthy subjects under 30 years of age (group 2). We calculated the following ratios for each voxel: N-acetyl-aspartate/creatine-phosphocreatine (NAA/Cr), N-acetyl-aspartate/choline (NAA/Cho), N-acetyl-aspartate /myoinositol (NAA/mI), choline/creatine-phosphocreatine (Cho/Cr), and myoinositol (mI/Cr). We compared the metabolic ratios in each region in each group and the correlation between age and the ratios within age ranges. Finally, we analyzed the differences in the metabolic ratios between groups and between sexes. Results. In group 1, we found negative correlations between age and Cho/Cr in the frontal region and NAA/mI in the temporal region. In group 2, we found negative correlations between age and mI/Cr and NAA/Cho in the temporal region as well as a positive correlation between age and NAA/mI in the temporal region. In the frontal lobe and the posteromedial region, NAA/Cr, NAA/Cho, and NAA/mI were lower in group 1 (P?0.003). No differences between groups were seen in Cho/Cr or mI/Cr. The values of the ratios differed regionally in all cases (P

Objective To determine the regional effects of age and sex on the metabolic ratios obtained in the medial temporal lobe, the posteromedial region, and the frontal lobe at 1.5 T single-voxel magnetic resonance spectroscopy. Material and methods We used single-voxel magnetic resonance spectroscopy to study the areas of the brain most affected in neurodegenerative disease (the left frontal lobe, the left medial temporal lobe, and the posteromedial region) in 31 healthy subjects older than 55 years of age (group 1) and in 20 healthy subjects under 30 years of age (group 2). We calculated the following ratios for each voxel: N-acetyl-aspartate/creatine-phosphocreatine (NAA/Cr), N-acetylaspartate/ choline (NAA/Cho), N-acetyl-aspartate /myoinositol (NAA/mI), choline/ creatine-phosphocreatine (Cho/Cr), and myoinositol (mI/Cr). We compared the metabolic ratios in each region in each group and the correlation between age and the ratios within age ranges. Finally, we analyzed the differences in the metabolic ratios between groups and between sexes. Results In group 1, we found negative correlations between age and Cho/Cr in the frontal region and NAA/mI in the temporal region. In group 2, we found negative correlations between age and mI/Cr and NAA/Cho in the temporal region as well as a positive correlation between age and NAA/mI in the temporal region. In the frontal lobe and the posteromedial region, NAA/ Cr, NAA/Cho, and NAA/mI were lower in group 1 (P ≤ 0.003). No differences between groups were seen in Cho/Cr or mI/Cr. The values of the ratios differed regionally in all cases (P Conclusions When using single-voxel magnetic resonance spectroscopy, especially in patients with neurodegenerative disease, variations due to region, age, and sex should always be taken into account.

The present research is aimed at assessing the role of 3 estrogen receptor alpha (ESR1) gene variants in late onset Alzheimer's disease (AD) susceptibility. One thousand one hundred thirteen unrelated late onset sporadic AD patients, 1109 healthy controls and 121 neurologically healthy elderly controls were used to carry out case-control genetic association studies with ESR1 rs3844508, rs2234693, and ESR1 noncoding deletion 1 (ESR1-NCD1) polymorphisms. Thirty-five healthy male samples were used for molecular analyses. The rs2234693 polymorphism is associated with AD in our population (odds ratio [OR], 1.29; p = 0.008). The rs3844508 marker confers protection against AD in males (OR, 0.57; p = 0.001) and the deletion ESR1-NCD1 is a risk factor for AD in women (OR, 1.67; p < 0.001). Molecular analyses on ESR1-NCD1 indicate that this deletion confers a higher response to estradiol activity on ESR1 receptor and it is also associated with differential expression of ESR1 isoforms. Our results support the involvement of ESR1 gene in AD and point to the existence of sexual dimorphism for ESR1 markers. In addition, carriers of ESR1-NCD1 deletion could overrespond to estradiol action.