Dallaire-Théroux Caroline, Callahan Brandy L, Potvin Olivier, Saikali Stéphan, Duchesne Simon
CERVO Brain Research Center, Institut Universitaire en Santé Mentale de Québec, Quebec City, Quebec, Canada.
Faculty of Medicine, Université Laval, Quebec City, Quebec, Canada.
J Alzheimers Dis. 2017;57(2):575-601. doi: 10.3233/JAD-161028.
The standard method of ascertaining Alzheimer's disease (AD) remains postmortem assessment of amyloid plaques and neurofibrillary degeneration. Vascular pathology, Lewy bodies, TDP-43, and hippocampal sclerosis are frequent comorbidities. There is therefore a need for biomarkers that can assess these etiologies and provide a diagnosis in vivo.
We conducted a systematic review of published radiological-pathological correlation studies to determine the relationship between antemortem magnetic resonance imaging (MRI) and neuropathological findings in AD.
We explored PubMed in June-July 2015 using "Alzheimer's disease" and combinations of radiological and pathological terms. After exclusion following screening and full-text assessment of the 552 extracted manuscripts, three others were added from their reference list. In the end, we report results based on 27 articles.
Independently of normal age-related brain atrophy, AD pathology is associated with whole-brain and hippocampal atrophy and ventricular expansion as observed on T1-weighted images. Moreover, cerebral amyloid angiopathy and cortical microinfarcts are also related to brain volume loss in AD. Hippocampal sclerosis and TDP-43 are associated with hippocampal and medial temporal lobe atrophy, respectively. Brain volume loss correlates more strongly with tangles than with any other pathological finding. White matter hyperintensities observed on proton density, T2-weighted and FLAIR images are strongly related to vascular pathologies, but are also associated with other histological changes such as gliosis or demyelination.
Cerebral atrophy and white matter changes in the living brain reflect underlying neuropathology and may be detectable using antemortem MRI. In vivo MRI may therefore be an avenue for AD pathological staging.
确定阿尔茨海默病（AD）的标准方法仍是对淀粉样斑块和神经纤维变性进行尸检评估。血管病变、路易体、TDP-43和海马硬化是常见的合并症。因此，需要能够评估这些病因并在体内进行诊断的生物标志物。
我们对已发表的放射学-病理学相关性研究进行了系统综述，以确定AD患者生前磁共振成像（MRI）与神经病理学发现之间的关系。
我们在2015年6月至7月期间使用“阿尔茨海默病”以及放射学和病理学术语的组合在PubMed上进行了检索。在对提取的552篇手稿进行筛选和全文评估后排除相关文献，另外从其参考文献列表中添加了3篇。最终，我们根据27篇文章报告结果。
与正常的年龄相关脑萎缩无关，AD病理学与T1加权图像上观察到的全脑和海马萎缩以及脑室扩大有关。此外，脑淀粉样血管病和皮质微梗死也与AD患者的脑容量损失有关。海马硬化和TDP-43分别与海马和内侧颞叶萎缩有关。脑容量损失与缠结的相关性比与任何其他病理学发现的相关性更强。在质子密度、T2加权和液体衰减反转恢复（FLAIR）图像上观察到的白质高信号与血管病变密切相关，但也与其他组织学变化如胶质增生或脱髓鞘有关。
活体大脑中的脑萎缩和白质变化反映了潜在的神经病理学，并且可以通过生前MRI检测到。因此，活体MRI可能是AD病理分期的一种途径。
