ارتباط شاخص توده بدنی و حجم کمتر لوب گیجگاهی در بیماری آلزایمر
Abstract
1- Introduction
2- Materials and methods
3- Results
4- Discussion
5- Conclusions
References
Abstract
1- Introduction
2- Materials and methods
3- Results
4- Discussion
5- Conclusions
References
Abstract
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.
Introduction
Alzheimer's disease (AD), the most common form of dementia, is a global health concern that places an epic burden on families, caregivers, healthcare systems, and the economy. An estimated 5.6 million Americans currently live with AD, and this number is expected to increase rapidly as the number of individuals over the age of 65 increases (Hebert et al., 2013). Brain changes, including atrophy and accumulation of β-amyloid peptide (Aβ) and tau, begin years before noticeable clinical and cognitive symptoms develop (Braak and Braak, 1991; Jack et al., 2013; Villemagne et al., 2013), making it imperative to investigate early risk factors that prevention methods could target to delay or prevent progression to AD. One variable that may play a role in development of AD is obesity. Obesity is a serious and growing health concern that impacts 38.9% of U.S. adults (Hales et al., 2018), and is associated with numerous deleterious health conditions, including diabetes and cardiovascular disease, as well as impaired quality of life (Dixon, 2010). One measure of obesity, body mass index (BMI), has a complex relationship with AD.
Abstract
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.
Introduction
Alzheimer's disease (AD), the most common form of dementia, is a global health concern that places an epic burden on families, caregivers, healthcare systems, and the economy. An estimated 5.6 million Americans currently live with AD, and this number is expected to increase rapidly as the number of individuals over the age of 65 increases (Hebert et al., 2013). Brain changes, including atrophy and accumulation of β-amyloid peptide (Aβ) and tau, begin years before noticeable clinical and cognitive symptoms develop (Braak and Braak, 1991; Jack et al., 2013; Villemagne et al., 2013), making it imperative to investigate early risk factors that prevention methods could target to delay or prevent progression to AD. One variable that may play a role in development of AD is obesity. Obesity is a serious and growing health concern that impacts 38.9% of U.S. adults (Hales et al., 2018), and is associated with numerous deleterious health conditions, including diabetes and cardiovascular disease, as well as impaired quality of life (Dixon, 2010). One measure of obesity, body mass index (BMI), has a complex relationship with AD.