Dr. Eduardo R. Zimmer, PhD, BPharm, Assistant Professor Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil, 90035-003, e-mail:
J Prev Alzheimers Dis. 2023;10(3):401-417. doi: 10.14283/jpad.2023.54.
In the past years, neuroinflammation has been widely investigated in Alzheimer's disease (AD). Evidence from animal, in vivo and post-mortem studies has shown that inflammatory changes are a common feature of the disease, apparently happening in response to amyloid-beta and tau accumulation. Progress in imaging and fluid biomarkers now allows for identifying surrogate markers of neuroinflammation in living individuals, which may offer unprecedented opportunities to better understand AD pathogenesis and progression. In this context, inflammatory mediators and glial proteins (mainly derived from microglial cells and astrocytes) seem to be the most promising biomarkers. Here, we discuss the biological basis of neuroinflammation in AD, revise the proposed neuroinflammation biomarkers, describe what we have learned from anti-inflammatory drug trials, and critically discuss the potential addition of these biomarkers in the AT(N) framework.
在过去的几年中,神经炎症在阿尔茨海默病(AD)中得到了广泛的研究。来自动物、体内和死后研究的证据表明,炎症变化是该疾病的一个共同特征,显然是对淀粉样蛋白-β和tau 积累的反应。成像和液体生物标志物的进展现在允许在活体个体中识别神经炎症的替代标志物,这可能为更好地了解 AD 的发病机制和进展提供前所未有的机会。在这种情况下,炎症介质和神经胶质蛋白(主要来自小胶质细胞和星形胶质细胞)似乎是最有前途的生物标志物。在这里,我们讨论了 AD 中神经炎症的生物学基础,修订了提出的神经炎症生物标志物,描述了我们从抗炎药物试验中学到的知识,并批判性地讨论了在 AT(N) 框架中添加这些标志物的潜力。