Department of Epidemiology, The George Washington University, Milken Institute School of Public Health, Washington, DC, USA.
Department of Epidemiology, The George Washington University, Milken Institute School of Public Health, Washington, DC, USA.
Neurobiol Aging. 2020 Aug;92:73-74. doi: 10.1016/j.neurobiolaging.2020.03.015. Epub 2020 Apr 15.
Elevated low-density lipoprotein cholesterol and total cholesterol in midlife and decline in total cholesterol from mid- to late-life are associated with incident dementia. Whether brain amyloid deposition mediates this relationship is unclear. We explored the association between midlife blood lipid levels and mid- to late-life change in lipid levels with brain amyloid deposition assessed using florbetapir PET scans in a biracial sample of 325 nondemented participants of the Atherosclerosis Risk in Communities-PET Amyloid Imaging study. Midlife total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides were not significantly associated with late-life amyloid burden after adjusting for covariates. Associations between changes in lipids and late-life amyloid deposition were similarly null. Lipids may contribute to dementia risk through alternate mechanisms.
中年时低密度脂蛋白胆固醇和总胆固醇升高,从中年到晚年总胆固醇水平下降与痴呆症的发生有关。但这种关系是否与脑淀粉样蛋白沉积有关尚不清楚。我们在动脉粥样硬化风险社区-PET 淀粉样蛋白成像研究的 325 名非痴呆参与者的双种族样本中,使用氟比他派 PET 扫描来评估脑淀粉样蛋白沉积,探讨了中年时的血脂水平与从中年到晚年的血脂水平变化与脑淀粉样蛋白沉积之间的关系。在校正协变量后,中年总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇和甘油三酯与晚年的淀粉样蛋白负担无显著相关性。脂质变化与晚年淀粉样蛋白沉积之间的相关性也同样为零。脂质可能通过其他机制导致痴呆症的风险。