Abstract：
Alzheimer\'s disease (AD) and Diabetes mellitus (DM) exhibit comparable pathophysiological pathways. Genetic abnormalities in APP, PS-1, and PS-2 are linked to AD, with diagnostic aid from CSF and blood biomarkers. Insulin dysfunction, termed \"type 3 diabetes mellitus\" in AD, involves altered insulin signalling and neuronal shrinkage. Insulin influences beta-amyloid metabolism, exacerbating neurotoxicity in AD and amyloid production in DM. Both disorders display impaired glucose transporter expression, hastening cognitive decline. Mitochondrial dysfunction and Toll-like receptor 4-mediated inflammation worsen neurodegeneration in both diseases. ApoE4 raises disease risk, especially when coupled with dyslipidemia common in DM. Targeting shared pathways like insulin-degrading enzyme activation and HSP60 holds promise for therapeutic intervention. Recognizing these interconnected mechanisms underscores the imperative for developing tailored treatments addressing the overlapping pathophysiology of AD and DM, offering potential avenues for more effective management of both conditions.
摘要：
阿尔茨海默病（AD）和糖尿病（DM）表现出可比的病理生理途径。APP中的遗传异常，PS-1和PS-2链接到AD，与CSF和血液生物标志物的诊断辅助。胰岛素功能障碍,在AD中被称为“3型糖尿病”，涉及胰岛素信号改变和神经元收缩。胰岛素影响β-淀粉样蛋白代谢，加剧AD的神经毒性和DM的淀粉样蛋白产生。两种疾病均显示葡萄糖转运蛋白表达受损，加速认知能力下降。线粒体功能障碍和Toll样受体4介导的炎症使两种疾病的神经变性恶化。ApoE4会增加疾病风险，特别是当伴有DM常见的血脂异常时。针对共享途径，如胰岛素降解酶激活和HSP60，有望进行治疗干预。认识到这些相互关联的机制强调了开发针对AD和DM的重叠病理生理学的定制治疗的必要性。为更有效地管理这两种情况提供了潜在的途径。
