Kim Sung-Woo, Kim Dong Ho, Hong Jin Yong, Mun Kyung-Ryoul, Jung Dawoon, Hong Ickpyo, Mc Ardle Ríona, Seong Joon-Kyung, Baek Min Seok
Department of Neurology, Wonju Severance Christian Hospital, Yonsei University Wonju College of Medicine, 20 Ilsan-ro, Wonju, Gangwon State, 26426, Republic of Korea.
Research Institute of Metabolism and Inflammation, Yonsei University Wonju College of Medicine, 20 Ilsan-ro, Wonju, Gangwon State, 26426, Republic of Korea.
Sci Rep. 2025 Feb 14;15(1):5539. doi: 10.1038/s41598-025-90020-4.
Research links gait impairment in Alzheimer's disease (AD) to cognitive abnormalities, brain atrophy, or amyloid-β (Aβ) deposition, with the exact cause unclear. This study investigated the relationship between gait, neuroimaging biomarkers, and cognition across the AD spectrum. We recruited 48 AD dementia patients, 27 with prodromal AD, and 41 cognitively unimpaired individuals, analyzing associations among gait parameters, cognitive scores, Aβ deposition, and cortical atrophy. Path and receiver operating characteristic (ROC) analyses evaluated gait impairment's interdependent interactions and diagnostic potential. Prodromal AD and AD dementia patients showed significantly slower gait pace than CU (p = 0.014 [velocity], p = 0.003 [step length]), linked to attention and executive functions, widespread Aβ deposition, and cortical atrophy, in the inferior parietal lobule, middle temporal gyrus, precuneus, and insula. Compared to CU, AD dementia patients exhibited greater gait variability and phase (p = 0.017 [step length standard deviation], p = 0.001 [double support percentage]), significantly correlated with cognition and Aβ deposition. Path analysis revealed a combined influence of Aβ deposition, cognitive impairment, and cortical atrophy on gait impairment, with > 80% observed gait impairments directly affected by Aβ deposition. ROC curves for diagnosing AD stages showed significant areas under the curve, suggesting gait characteristics as noninvasive biomarkers for early AD diagnosis and progression monitoring.
研究将阿尔茨海默病（AD）中的步态障碍与认知异常、脑萎缩或淀粉样β蛋白（Aβ）沉积联系起来，但其确切原因尚不清楚。本研究调查了整个AD谱系中步态、神经影像学生物标志物与认知之间的关系。我们招募了48名AD痴呆患者、27名前驱AD患者和41名认知未受损个体，分析了步态参数、认知分数、Aβ沉积和皮质萎缩之间的关联。路径分析和受试者工作特征（ROC）分析评估了步态障碍的相互依存关系和诊断潜力。前驱AD和AD痴呆患者的步态速度明显慢于认知未受损个体（p = 0.014[速度]，p = 0.003[步长]），这与注意力和执行功能、广泛的Aβ沉积以及顶下小叶、颞中回、楔前叶和脑岛的皮质萎缩有关。与认知未受损个体相比，AD痴呆患者表现出更大的步态变异性和相位（p = 0.017[步长标准差]，p = 0.001[双支撑百分比]），与认知和Aβ沉积显著相关。路径分析显示，Aβ沉积、认知障碍和皮质萎缩对步态障碍有综合影响，超过80%观察到的步态障碍直接受Aβ沉积影响。用于诊断AD阶段的ROC曲线显示曲线下面积显著，表明步态特征可作为早期AD诊断和病情进展监测的非侵入性生物标志物。
