Honea Robyn A, John Casey S, Green Zachary D, Kueck Paul J, Taylor Matthew K, Lepping Rebecca J, Townley Ryan, Vidoni Eric D, Burns Jeffery M, Morris Jill K
University of Kansas Alzheimer's Disease Research Center Kansas City Kansas USA.
Department of Neurology University of Kansas Medical Center Kansas City Kansas USA.
Alzheimers Dement (N Y). 2022 Feb 1;8(1):e12239. doi: 10.1002/trc2.12239. eCollection 2022.
Fasting glucose increases with age and is linked to modifiable Alzheimer's disease risk factors such as cardiovascular disease and Type 2 diabetes (T2D).
We leveraged available biospecimens and neuroimaging measures collected during the Alzheimer's Prevention Through Exercise (APEx) trial (n = 105) to examine the longitudinal relationship between change in blood glucose metabolism and change in regional cerebral amyloid deposition and gray and white matter (WM) neurodegeneration in older adults over 1 year of follow-up.
Individuals with improving fasting glucose (n = 61) exhibited less atrophy and regional amyloid accumulation compared to those whose fasting glucose worsened over 1 year (n = 44). Specifically, while individuals with increasing fasting glucose did not yet show cognitive decline, they did have regional atrophy in the hippocampus and inferior parietal cortex, and increased amyloid accumulation in the precuneus cortex. Signs of early dementia pathology occurred in the absence of significant group differences in insulin or body composition, and was not modified by apolipoprotein E ε4 carrier status.
Dysregulation of glucose in late life may signal preclinical brain change prior to clinically relevant cognitive decline. Additional work is needed to determine whether treatments specifically targeting fasting glucose levels may impact change in brain structure or cerebral amyloid in older adults.
空腹血糖随年龄增长而升高，且与心血管疾病和2型糖尿病（T2D）等可改变的阿尔茨海默病风险因素相关。
我们利用在通过运动预防阿尔茨海默病（APEx）试验期间收集的现有生物样本和神经影像学测量数据（n = 105），来研究老年人在1年随访期间血糖代谢变化与局部脑淀粉样蛋白沉积变化以及灰质和白质（WM）神经变性之间的纵向关系。
与空腹血糖在1年内恶化的个体（n = 44）相比，空腹血糖改善的个体（n = 61）表现出较少的萎缩和局部淀粉样蛋白积累。具体而言，虽然空腹血糖升高的个体尚未出现认知衰退，但他们在海马体和顶下小叶皮质出现了局部萎缩，并且楔前叶皮质的淀粉样蛋白积累增加。早期痴呆病理迹象在胰岛素或身体组成方面无显著组间差异的情况下出现，且不受载脂蛋白E ε4携带者状态的影响。
晚年血糖失调可能预示着在临床相关认知衰退之前的临床前脑变化。需要进一步的研究来确定专门针对空腹血糖水平的治疗是否可能影响老年人的脑结构或脑淀粉样蛋白变化。
