A 74-year-old woman with mild Alzheimer disease joined a clinical trial of anti–amyloid-β therapy. Three weeks after receiving remternetug, a N3pH-Aβ monoclonal antibody, a scheduled brain MRI showed new periventricular and subcortical FLAIR hyperintensities (Figure, A) suggestive of mild amyloid-related imaging abnormalities (ARIA).^1,2 Two weeks later, she was hospitalized for rapid cognitive and functional decline. Her admission examination was notable for severe disorientation, inattention, and global aphasia. Repeat MRI showed diffuse and confluent FLAIR hyperintensities consistent with progression to severe ARIA-edema/effusion (ARIA-E), but no hemosiderosis/microhemorrhages (ARIA-H) (Figure, B). She was treated with steroids and continued to have a gradual improvement in her cognition and language. A follow-up MRI 6 weeks later showed a marked reduction in FLAIR hyperintensities (Figure, C). In clinical trials, ARIA-E has often been observed to improve within 3–4 months.² Early suspicion of ARIAs is essential for identifying and managing this adverse effect of anti–amyloid-β therapy.

一名患有轻度阿尔茨海默病的 74 岁女性参加了抗淀粉样蛋白治疗的临床试验。接受 remternetug（一种 N3pH-Aβ 单克隆抗体）三周后，预定的脑 MRI 显示新的脑室周围和皮质下 FLAIR 高信号（图 A），提示轻度淀粉样蛋白相关成像异常 (ARIA)。^1,2两周后，她因认知和功能快速下降而住院。她的入院检查因严重迷失方向、注意力不集中和全面失语而引人注目。重复 MRI 显示弥漫性和汇合性 FLAIR 高信号，与进展为严重 ARIA 水肿/积液 (ARIA-E) 一致，但没有含铁血黄素沉着/微出血 (ARIA-H)（图 B）。她接受了类固醇治疗，认知和语言能力逐渐改善。6 周后的随访 MRI 显示 FLAIR 高信号显着降低（图 C）。在临床试验中，经常观察到 ARIA-E 在 3-4 个月内得到改善。²早期怀疑 ARIA 对于识别和管理抗淀粉样蛋白治疗的这种不良反应至关重要。