Hippocampal volume is related to body mass index in Alzheimer's disease.
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ABSTRACT:
SUBMITTER: Ho AJ
PROVIDER: S-EPMC3197837 | biostudies-literature | 2011 Jan
REPOSITORIES: biostudies-literature
Publications
Hippocampal volume is related to body mass index in Alzheimer's disease.
Ho April J AJ Raji Cyrus A CA Saharan Priya P DeGiorgio Andrew A Madsen Sarah K SK Hibar Derrek P DP Stein Jason L JL Becker James T JT Lopez Oscar L OL Toga Arthur W AW Thompson Paul M PM
Neuroreport 20110101 1
Obesity is associated with lower brain volumes in early Alzheimer's disease, but its effects on hippocampal volumes are unclear, as weight loss is also associated with Alzheimer's disease. To address this question, we applied an automated hippocampal mapping method to brain MRI scans for 162 patients with Alzheimer's disease. We hypothesized that obesity, measured by body mass index, would be associated with lower hippocampal volumes in mildly affected patients. Statistical maps showed a selecti ...[more]
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Project description:ObjectiveThis study aims to explore whether body mass index (BMI) level affects the executive function and hippocampal subregion volume of subjective cognitive decline (SCD).Materials and methodsA total of 111 participants were included in the analysis, including SCD (38 of normal BMI, 27 of overweight and obesity) and normal cognitive control (NC) (29 of normal BMI, 17 of overweight and obesity). All subjects underwent the Chinese version of the Stroop Color-Word Test (SCWT) to measure the executive function and a high-resolution 3D T1 structural image acquisition. Two-way ANOVA was used to examine the differences in executive function and gray matter volume in hippocampal subregions under different BMI levels between the SCD and NC.ResultThe subdimensions of executive function in which different BMI levels interact with SCD and NC include inhibition control function [SCWT C-B reaction time(s): F (1,104) = 5.732, p = 0.018], and the hippocampal subregion volume of CA1 [F (1,99) = 8.607, p = 0.004], hippocampal tail [F (1,99) = 4.077, p = 0.046], and molecular layer [F (1,99) = 6.309, p = 0.014]. After correction by Bonferroni method, the population × BMI interaction only had a significant effect on the CA1 (p = 0.004). Further analysis found that the SCWT C-B reaction time of SCD was significantly longer than NC no matter whether it is at the normal BMI level [F (1,104) = 4.325, p = 0.040] or the high BMI level [F (1,104) = 21.530, p < 0.001], and the inhibitory control function of SCD was worse than that of NC. In the normal BMI group, gray matter volume in the hippocampal subregion (CA1) of SCD was significantly smaller than that of NC [F (1,99) = 4.938, p = 0.029]. For patients with SCD, the high BMI group had worse inhibitory control function [F (1,104) = 13.499, p < 0.001] and greater CA1 volume compared with the normal BMI group [F (1,99) = 7.619, p = 0.007].ConclusionThe BMI level is related to the inhibition control function and the gray matter volume of CA1 subregion in SCD. Overweight seems to increase the gray matter volume of CA1 in the elderly with SCD, but it is not enough to compensate for the damage to executive function caused by the disease. These data provide new insights into the relationship between BMI level and executive function of SCD from the perspective of imaging.
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Project description:Body mass index (BMI) has a complex relationship with Alzheimer's disease (AD); in midlife, high BMI is associated with increased risk for AD, whereas the relationship in late-life is still unclear. To clarify the relationship between late-life BMI and risk for AD, this study examined the extent to which genetic predisposition for AD moderates BMI and AD-related biomarker associations. Participants included 126 cognitively normal older adults at baseline from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. Genetic risk for AD was assessed via polygenic hazard score. AD-related biomarkers assessed were medial temporal lobe volume and cerebrospinal fluid (CSF) biomarkers. Hierarchical linear regressions were implemented to examine the effects of BMI and polygenic hazard score on AD-related biomarkers. Results showed that BMI moderated the relationship between genetic risk for AD and medial temporal lobe volume, such that individuals with high BMI and high genetic risk for AD showed lower volume in the entorhinal cortex and hippocampus. In sex-stratified analyses, these results remained significant only in females. Finally, BMI and genetic risk for AD were independently associated with CSF biomarkers of AD. These results provide evidence that high BMI is associated with lower volume in AD-vulnerable brain regions in individuals at genetic risk for AD, particularly females. The genetic pathways of AD may be exacerbated by high BMI. Environmental and genetic risk factors rarely occur in isolation, which underscores the importance of looking at their synergistic effects, as they provide insight into early risk factors for AD that prevention methods could target.
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Project description:Observational research shows that higher body mass index (BMI) increases Alzheimer's disease (AD) risk, but it is unclear whether this association is causal. We applied genetic variants that predict BMI in Mendelian randomization analyses, an approach that is not biased by reverse causation or confounding, to evaluate whether higher BMI increases AD risk. We evaluated individual-level data from the AD Genetics Consortium (ADGC: 10,079 AD cases and 9613 controls), the Health and Retirement Study (HRS: 8403 participants with algorithm-predicted dementia status), and published associations from the Genetic and Environmental Risk for AD consortium (GERAD1: 3177 AD cases and 7277 controls). No evidence from individual single-nucleotide polymorphisms or polygenic scores indicated BMI increased AD risk. Mendelian randomization effect estimates per BMI point (95% confidence intervals) were as follows: ADGC, odds ratio (OR) = 0.95 (0.90-1.01); HRS, OR = 1.00 (0.75-1.32); GERAD1, OR = 0.96 (0.87-1.07). One subscore (cellular processes not otherwise specified) unexpectedly predicted lower AD risk.
| S-EPMC4676945 | biostudies-literature
Project description:The effect of body mass index (BMI) changes and variability on the risk for Alzheimer's disease (AD) remains unclear. We analyzed 45,076 participants, whose BMI were measured on phase 1 (2002-2003), phase 2 (2004-2005), and phase 3 (2006-2007), of the Korean National Health Insurance Service-Health Screening Cohort. We evaluated the effect of 2- and 4-year BMI changes and BMI variability on the risk of AD using Cox regression models. In men, association between 2-year BMI changes, BMI variability, and the risk of AD was not significant. Risk of AD was higher in men whose BMI had decreased 10.1-15.0% over 4 years. In women, aHRs and 95% CIs for AD were 1.14 (1.02-1.29), 1.44 (1.17-1.79), and 1.51 (1.09-2.09) when 2-year BMI loss was 5.1-10.0%, 10.1-15.0%, and > 15.0%. The HRs for AD in women significantly increased when 4-year BMI loss was > 5.0%. The aHR and 95% CI for AD was 1.31 (1.17-1.46) in the 4th quartile of average successive variability (ASV) compared with the 1st quartile of ASV in women. BMI loss over 2- and 4-year period was associated with increased risk for AD, and risk increased in women with higher BMI variability. Appropriate body weight management is recommended to prevent AD.
| S-EPMC7862316 | biostudies-literature
Project description:BackgroundSpinocerebellar ataxias (SCAs) are dominantly inherited, progressive ataxia disorders. Disease progression could be preceded by weight loss.ObjectivesWe aimed to study the course of weight loss in patients who had the most common SCAs (SCA1, SCA2 SCA3, and SCA6). Additional objectives were to identify subgroups of weight evolution, to determine the factors influencing these evolutions, and to assess the impact of these evolutions on disease progression.MethodsIn total, 384 patients from the EUROSCA prospective cohort study were analyzed who had SCA1, SCA2, SCA3, or SCA6 and at least 3 measurements of weight. Age was used as a time scale. Clinical outcomes were body mass index (BMI) and the Scale for the Assessment and Rating Ataxia (SARA), with scores ranging from 0 to 40. We used a linear mixed model to analyze the course of BMI and a latent class mixed model to identify subgroup BMI evolution.ResultsOverall, BMI declined over time (-0.11 ± 0.03 kg/m2 per decade; P = 0.0009). Three subgroups of BMI evolution were identified: "decreasing BMI" (n = 88; 23%), "increasing BMI" (n = 70; 18%) and "stable BMI" (n = 226; 59%). Patients in the decreasing BMI group were more severely affected at baseline with higher SARA scores and a higher frequency of non-ataxia signs (especially motor symptoms) compared with those in the other groups. Weight loss was associated with faster disease progression (5.7 ± 0.7 SARA points per decade; P = 0.036).ConclusionsThe current data have substantial implications for the design of future interventional studies in SCA, as they provide a basis for patient stratification and emphasize the usefulness of BMI as a biomarker for monitoring disease progression.
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Project description:Background and objectives18-kDa translocator protein position-emission-tomography (TSPO-PET) imaging emerged for in vivo assessment of neuroinflammation in Alzheimer's disease (AD) research. Sex and obesity effects on TSPO-PET binding have been reported for cognitively normal humans (CN), but such effects have not yet been systematically evaluated in patients with AD. Thus, we aimed to investigate the impact of sex and obesity on the relationship between β-amyloid-accumulation and microglial activation in AD.Methods49 patients with AD (29 females, all Aβ-positive) and 15 Aβ-negative CN (8 female) underwent TSPO-PET ([18F]GE-180) and β-amyloid-PET ([18F]flutemetamol) imaging. In 24 patients with AD (14 females), tau-PET ([18F]PI-2620) was additionally available. The brain was parcellated into 218 cortical regions and standardized-uptake-value-ratios (SUVr, cerebellar reference) were calculated. Per region and tracer, the regional increase of PET SUVr (z-score) was calculated for AD against CN. The regression derived linear effect of regional Aβ-PET on TSPO-PET was used to determine the Aβ-plaque-dependent microglial response (slope) and the Aβ-plaque-independent microglial response (intercept) at the individual patient level. All read-outs were compared between sexes and tested for a moderation effect of sex on associations with body mass index (BMI).ResultsIn AD, females showed higher mean cortical TSPO-PET z-scores (0.91 ± 0.49; males 0.30 ± 0.75; p = 0.002), while Aβ-PET z-scores were similar. The Aβ-plaque-independent microglial response was stronger in females with AD (+ 0.37 ± 0.38; males with AD - 0.33 ± 0.87; p = 0.006), pronounced at the prodromal stage. On the contrary, the Aβ-plaque-dependent microglial response was not different between sexes. The Aβ-plaque-independent microglial response was significantly associated with tau-PET in females (Braak-II regions: r = 0.757, p = 0.003), but not in males. BMI and the Aβ-plaque-independent microglial response were significantly associated in females (r = 0.44, p = 0.018) but not in males (BMI*sex interaction: F(3,52) = 3.077, p = 0.005).ConclusionWhile microglia response to fibrillar Aβ is similar between sexes, women with AD show a stronger Aβ-plaque-independent microglia response. This sex difference in Aβ-independent microglial activation may be associated with tau accumulation. BMI is positively associated with the Aβ-plaque-independent microglia response in females with AD but not in males, indicating that sex and obesity need to be considered when studying neuroinflammation in AD.
| S-EPMC10804830 | biostudies-literature
Project description:ContextRecently, data on 2,000,000 people established that low body mass index (BMI) is associated with increased risk of dementia. Whether this observational association reflects a causal effect remains to be clarified.ObjectiveWe tested the hypothesis that there is a causal association between low BMI and high risk of Alzheimer's disease.Design, setting, and participantsUsing a Mendelian randomization approach, we studied 95,578 individuals from the Copenhagen General Population Study (CGPS) with up to 36 years of follow-up and consortia data on 303,958 individuals from the Genetic Investigation of Anthropometric Traits (GIANT) and the International Genomics of Alzheimer's Project (IGAP).Main outcome measureRisk of Alzheimer's disease.ResultsThe causal odds ratio for a 1-kg/m2 genetically determined lower BMI was 0.98 [95% confidence interval (CI), 0.77 to 1.23] for a weighted allele score in the CGPS. Using 32 BMI-decreasing variants from GIANT and IGAP the causal odds ratio for Alzheimer's disease for a 1-standard deviation (SD) lower genetically determined BMI was 1.02 (95% CI, 0.86 to 1.22). Corresponding observational hazard ratios from the CGPS were 1.07 (95% CI, 1.05 to 1.09) and 1.32 (95% CI, 1.20 to 1.46) for a 1-kg/m2 and a 1-SD lower BMI, respectively.ConclusionsGenetic and hence lifelong low BMI is not associated with increased risk of Alzheimer's disease in the general population. These data suggest that low BMI is not a causal risk factor for Alzheimer's disease and that the corresponding observational association likely is explained by reverse causation or confounding.
| S-EPMC5505195 | biostudies-literature
Project description:Background and aimsAn independent association of body mass index (BMI) with atherosclerotic cardiovascular disease is somewhat controversial and may differ by vascular bed. Sex-specific risk factors for atherosclerosis may further modify these associations. Obesity and peripheral artery disease (PAD) are both more prevalent in women. We sought to determine the association between PAD and BMI using a very large population-based study.MethodsSelf-referred individuals at >20,000 US sites completed medical questionnaires including height and weight, and were evaluated by screening ankle brachial indices (ABI) for PAD (ABI<0.9).ResultsAmong 3,250,350 individuals, the mean age was 63.1 ± 10.5 years and 65.5% were women. The mean BMI was 27.7 ± 5.8 kg/m2. 27.8% of participants were obese (BMI ≥30 kg/m2) - 27.6% females, 28.1% males. Overweight individuals (BMI 25-29.9 kg/m2) exhibited the lowest prevalence of PAD. There was a J-shaped association of BMI with prevalent PAD. After adjustment for age and cardiovascular risk factors, underweight was associated with similarly increased odds of PAD (1.72 vs. 1.39, women and men, respectively). The association of obesity with PAD was predominant in women, with only a slight association of increasing BMI with PAD in men (OR = 2.98 vs. 1.37 for BMI ≥40 kg/m2).ConclusionsOur study suggests that increasing BMI is a robust independent risk factor for PAD only in women. This observation requires validation, but highlights the need for further research on sex-specific risk and mechanisms of atherosclerosis.
| S-EPMC6981229 | biostudies-literature