Departmen of Basic Medical Sciences, College of Medicine, University of Sharjah, Sharjah, United Arab Emirates; Cardiovascular Research Group, Research Institute of Medical and Health Science, University of Sharjah, Sharjah, United Arab Emirates.
Department of Neurology and Stroke Medicine, Rehman Medical Institute, Peshawar, Pakistan.
Arch Med Res. 2024 Jul;55(5):103025. doi: 10.1016/j.arcmed.2024.103025. Epub 2024 Jun 16.
Sarcopenia or age-associated muscle loss is common in patients with Alzheimer's disease (AD). We have previously demonstrated the contribution of a leaky gut to sarcopenia in AD. Here, we asked whether resistant exercise (RE) reduces the sarcopenia phenotype by repairing intestinal leakage in patients with AD.
A prospective, single-center study of older adults, including healthy controls and patients with AD (n = 44-51/group), was conducted to measure plasma zonulin and claudin-3 (markers of intestinal leakage), handgrip strength (HGS), and short physical performance battery (SPPB) as a measure of functional capacity. Measurements in patients with AD were performed at baseline and after 12 weeks of RE.
At baseline, patients with AD had higher plasma zonulin and claudin-3 and lower HGS, gait speed, and SPPB scores than controls. RE reduced plasma zonulin and claudin-3 levels and improved HGS, SPPB scores, and gait speed. Regression analysis revealed robust relationships between changes in plasma zonulin and claudin-3 with HGS. Plasma zonulin was also positively associated with SPPB scores. In addition, RE downregulated plasma markers of inflammation and oxidative stress. However, the prevalence of sarcopenia based on low HGS and muscle atrophy or low SPPB was not affected by RE.
Taken together, disruption of the intestinal mucosal barrier may contribute to functional decline and sarcopenia in AD, which is incompletely recovered by RE. Circulating levels of zonulin and claudin-3 may be valuable in predicting sarcopenia and functional capacity in older adults with AD.
肌肉减少症或与年龄相关的肌肉丢失在阿尔茨海默病（AD）患者中很常见。我们之前已经证明肠道渗漏对 AD 中肌肉减少症的贡献。在这里，我们询问抵抗运动（RE）是否通过修复 AD 患者的肠道渗漏来减少肌肉减少症表型。
对包括健康对照者和 AD 患者在内的老年人进行了一项前瞻性、单中心研究（每组 44-51 名），以测量血浆肠通透素和紧密连接蛋白-3（肠道渗漏的标志物）、握力（HGS）和简短体能测试（SPPB）作为功能能力的衡量标准。在 AD 患者中，在基线和 RE 后 12 周进行测量。
在基线时，AD 患者的血浆肠通透素和紧密连接蛋白-3水平较高，HGS、步态速度和 SPPB 评分较低。RE 降低了血浆肠通透素和紧密连接蛋白-3水平，提高了 HGS、SPPB 评分和步态速度。回归分析显示，血浆肠通透素和紧密连接蛋白-3的变化与 HGS 之间存在稳健的关系。血浆肠通透素与 SPPB 评分呈正相关。此外，RE 下调了血浆炎症和氧化应激标志物。然而，基于低 HGS 和肌肉萎缩或低 SPPB 的肌肉减少症患病率不受 RE 影响。
综上所述，肠道黏膜屏障的破坏可能导致 AD 患者的功能下降和肌肉减少症，RE 不能完全恢复。循环中的肠通透素和紧密连接蛋白-3水平可能对预测 AD 老年患者的肌肉减少症和功能能力有价值。
