Goodman Max J, Li Xin Ran, Livschitz Jennifer, Huang Chiang-Ching, Bendlin Barbara B, Granadillo Elias D
Medical College of Wisconsin, Wauwatosa, WI, USA.
University of Wisconsin, Madison, WI, USA.
J Alzheimers Dis Rep. 2023 Dec 29;7(1):1427-1444. doi: 10.3233/ADR-230054. eCollection 2023.
Physicians may soon be able to diagnose Alzheimer's disease (AD) in its early stages using fluid biomarkers like amyloid. However, it is acknowledged that additional biomarkers need to be characterized which would facilitate earlier monitoring of AD pathogenesis.
To determine if a potential novel inflammation biomarker for AD, symmetric dimethylarginine, has utility as a baseline serum biomarker for discriminating prodromal AD from cognitively unimpaired controls in comparison to cerebrospinal fluid amyloid-β42 (Aβ).
Data including demographics, magnetic resonance imaging and fluorodeoxyglucose-positron emission tomography scans, Mini-Mental State Examination and Functional Activities Questionnaire scores, and biomarker concentrations were obtained from the Alzheimer's Disease Neuroimaging Initiative for a total of 146 prodromal AD participants and 108 cognitively unimpaired controls.
Aβ ( = 0.65) and symmetric dimethylarginine ( = 0.45) were unable to predict age-matched cognitively unimpaired controls and prodromal AD participants. Aβ was negatively associated with regional brain atrophy and hypometabolism as well as cognitive and functional decline in cognitively unimpaired control participants ( < 0.05) that generally decreased in time. There were no significant associations between Aβ and symmetric dimethylarginine with imaging or neurocognitive biomarkers in prodromal AD patients.
Correlations were smaller between Aβ and neuropathological biomarkers over time and were absent in prodromal AD participants, suggesting a plateau effect dependent on age and disease stage. Evidence supporting symmetric dimethylarginine as a novel biomarker for AD as a single measurement was not found.
医生或许很快就能利用诸如淀粉样蛋白等体液生物标志物在早期阶段诊断阿尔茨海默病（AD）。然而，人们认识到需要对其他生物标志物进行特征描述，这将有助于更早地监测AD的发病机制。
确定一种潜在的AD新型炎症生物标志物——对称二甲基精氨酸，与脑脊液淀粉样蛋白-β42（Aβ）相比，是否可用作基线血清生物标志物，以区分前驱AD与认知未受损的对照者。
从阿尔茨海默病神经影像倡议组织获取了包括人口统计学数据、磁共振成像和氟脱氧葡萄糖-正电子发射断层扫描、简易精神状态检查表和功能活动问卷得分以及生物标志物浓度等数据，共有146名前驱AD参与者和108名认知未受损对照者。
Aβ（=0.65）和对称二甲基精氨酸（=0.45）无法预测年龄匹配的认知未受损对照者和前驱AD参与者。在认知未受损对照参与者中，Aβ与脑区萎缩、代谢减退以及认知和功能衰退呈负相关（<0.05），且这些指标通常随时间下降。在前驱AD患者中，Aβ和对称二甲基精氨酸与影像学或神经认知生物标志物之间无显著关联。
随着时间推移，Aβ与神经病理学生物标志物之间的相关性较小，在前驱AD参与者中不存在这种相关性，这表明存在依赖于年龄和疾病阶段的平台效应。未发现支持对称二甲基精氨酸作为AD单一测量新型生物标志物的证据。
