Progressive aphasia secondary to Alzheimer disease vs FTLD pathology
Progressive aphasia secondary to Alzheimer disease vs FTLD pathology
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DOI：
10.1212/01.wnl.0000287073.12737.35
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发表时间：
2008-01-01
期刊：
影响因子：
9.9
通讯作者：
Petersen, R. C.
中科院分区：
文献类型：
--
作者：
Josephs, K. A.;Whitwell, J. L.;Petersen, R. C.
背景：导致进行性失语的病理是一种典型的额颞叶变性，特别是泛素阳性包涵体（FTLD-U）。不太常见的潜在病理是阿尔茨海默病（AD）。目的：比较进行性失语伴AD病理患者与失语伴FTLD-U病理患者及典型AD患者的临床病理及MRI特征。方法：从216例失语症患者中，通过MRI鉴定5例失语症合并AD病理，5例失语症合并FTLD-U病理。10名受试者具有典型的阿尔茨海默病临床特征和阿尔茨海默病病理。所有AD病理患者均行TDP-43免疫组织化学病理再分析。采用体素形态测定法（VBM）对伴有AD病理的失语症患者、伴有FTLD-U的失语症患者和伴有AD病理的典型AD患者的灰质萎缩模式进行评估，并与正常对照组进行比较。结果：所有失语者均有流利的言语输出。然而，AD病理组的处理速度优于FTLD-U病理组。免疫组化TDP-43抗体阴性。VBM显示灰质萎缩主要发生在颞顶皮质，而AD失语症患者的海马明显保留。相比之下，患有FTLD-U的失语症患者表现出顶叶的保留。典型AD患者表现为颞顶和海马萎缩。结论：进行性流利性失语患者的MRI颞顶叶萎缩模式和相对保存的处理速度提示潜在的阿尔茨海默病病理，而不是泛素免疫反应性改变的额颞叶变性。
Background: The pathology causing progressive aphasia is typically a variant of frontotemporal lobar degeneration, especially with ubiquitin-positive inclusions (FTLD-U). Less commonly the underlying pathology is Alzheimer disease (AD).Objective: To compare clinicopathologic and MRI features of subjects with progressive aphasia and AD pathology to subjects with aphasia and FTLD-U pathology and subjects with typical AD.Methods: We identified 5 subjects with aphasia and AD pathology and 5 with aphasia and FTLD-U pathology with an MRI from a total of 216 aphasia subjects. Ten subjects with typical AD clinical features and AD pathology were also identified. All subjects with AD pathology underwent pathologic reanalysis with TDP-43 immunohistochemistry. Voxel-based morphometry (VBM) was used to assess patterns of gray matter atrophy in the aphasia cases with AD pathology, aphasia cases with FTLD-U, and typical AD cases with AD pathology, compared with a normal control group.Results: All aphasic subjects had fluent speech output. However, those with AD pathology had better processing speed than those with FTLD-U pathology. Immunohistochemistry with TDP-43 antibodies was negative. VBM revealed gray matter atrophy predominantly in the temporoparietal cortices, with notable sparing of the hippocampus in the aphasia with AD subjects. In comparison, the aphasic subjects with FTLD-U showed sparing of the parietal lobe. Typical AD subjects showed temporoparietal and hippocampal atrophy.Conclusions: A temporoparietal pattern of atrophy on MRI in patients with progressive fluent aphasia and relatively preserved processing speed is suggestive of underlying Alzheimer disease pathology rather than frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes.