Geng Zhao, Yu Zhong-Yuan, Tan Jun, Wang Xuan-Yue, Zeng Gui-Hua, Li Jiang-Hui, Bai Yu-Di, Zeng Xiao-Qin, Zhu Yu-Peng, Tan Cheng-Rong, Shi An-Yu, Liu Yu-Hui, Bu Xian-Le, Ye Zi, Wang Yan-Jiang, Li Zhao-Hui
Senior Department of Ophthalmology, The Third Medical Centre of PLA General Hospital, Beijing, 100853, China.
Department of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Neurosci Bull. 2025 Jun 28. doi: 10.1007/s12264-025-01442-z.
Clinical investigations have suggested a potential link between cataracts and Alzheimer's disease (AD). However, whether cataract has an impact on the progression of AD remains unclear. The objective of this research was to determine the relationship between cataracts and AD. A cataract model was established in APP/PS1 [mutant amyloid precursor protein (APP) and a mutant presenilin-1 (PS1) gene] mice via lens puncture. Behavioural assays were used to evaluate cognitive function. Immunohistochemistry, immunofluorescence, and enzyme-linked immunosorbent assays (ELISA) were applied to detect AD-related pathology. Visual signals were markedly obstructed following surgery to induce cataracts, and these mice presented an increased cerebral amyloid-beta (Aβ) load, while no significant alterations in the levels of enzymes associated with Aβ metabolism were detected. In addition, compared with control mice, cataract model mice presented increased astrogliosis and microgliosis, along with elevated levels of proinflammatory factors. Moreover, cataract model mice presented more pronounced cognitive impairments than did control mice. Our study offers experimental confirmation that cataract considerably contributes to the pathogenesis of AD, thereby emphasizing the importance of visual signals in maintaining cognitive well-being.
临床研究表明白内障与阿尔茨海默病（AD）之间可能存在联系。然而，白内障是否会对AD的进展产生影响仍不清楚。本研究的目的是确定白内障与AD之间的关系。通过晶状体穿刺在APP/PS1[突变淀粉样前体蛋白（APP）和突变早老素-1（PS1）基因]小鼠中建立白内障模型。采用行为学实验评估认知功能。应用免疫组织化学、免疫荧光和酶联免疫吸附测定（ELISA）检测AD相关病理学变化。诱导白内障手术后视觉信号明显受阻，这些小鼠脑内β淀粉样蛋白（Aβ）负荷增加，而未检测到与Aβ代谢相关酶水平的显著变化。此外，与对照小鼠相比，白内障模型小鼠出现星形胶质细胞增生和小胶质细胞增生增加，同时促炎因子水平升高。而且，白内障模型小鼠比对照小鼠表现出更明显的认知障碍。我们的研究提供了实验证据，证明白内障对AD的发病机制有很大影响，从而强调了视觉信号在维持认知健康方面的重要性。
