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偶然发现的 C9orf72 扩展突变相关额颞叶变性病理学和散发性克雅氏病。

Co-incidental C9orf72 expansion mutation-related frontotemporal lobar degeneration pathology and sporadic Creutzfeldt-Jakob disease.

机构信息

Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria.

Austrian Reference Center for Human Prion Diseases (OERPE), Vienna, Austria.

出版信息

Eur J Neurol. 2021 Mar;28(3):1009-1015. doi: 10.1111/ene.14621. Epub 2020 Dec 1.

Abstract

BACKGROUND

The C9orf72 hexanucleotide expansion mutation is the most common cause of genetic frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS) and combined FTD-ALS. Its underlying neuropathology combines TDP-43 pathology and dipeptide repeat protein (DPR) deposits and may also associate with other neurodegeneration-associated protein aggregates. Herein we present a unique combination of C9orf72 mutation with sporadic Creutzfeldt-Jakob disease (CJD) in a 74-year-old patient with rapidly progressive dementia.

METHODS

Detailed neuropathological examination including immunohistochemistry for several proteinopathies. Genetic analysis was conducted by repeat primed polymerase chain reaction (PCR). Furthermore, we analyzed additional C9orf72 mutation carriers for prion-protein (PrP) deposits in brain tissue and screened the cerebellar cortex of other CJD cases for p62/DPR neuronal inclusions to assess the frequency of combined pathologies.

RESULTS

Postmortem brain examination of a patient with a rapidly progressive neurological deterioration of 8 months' duration confirmed the diagnosis of CJD. She harbored valine homozygosity at PRNP codon 129. In addition, a frontotemporal lobar degeneration (FTLD)-pattern with TDP-43 protein aggregates and p62+/C9RANT+ positive inclusions along with a high degree of Alzheimer-related pathology (A3B3C3) were identified. The suspected C9orf72 expansion mutation was confirmed by repeat-primed PCR. Screening of 13 C9orf72 cases showed no pathological PrP aggregates and screening of 100 CJD cases revealed no other C9orf72 expansion mutation carriers.

CONCLUSION

A combination of a C9orf72 expansion mutation-related FTLD with sporadic CJD in the same patient is rare. While the rarity of both diseases makes this concurrence most likely to be coincidental, questions regarding a potential link between these two neurodegenerative pathologies deserve further studies.

摘要

背景

C9orf72 六核苷酸扩展突变是遗传性额颞叶痴呆(FTD)、肌萎缩侧索硬化症(ALS)和 FTD-ALS 合并症的最常见原因。其潜在的神经病理学结合 TDP-43 病理学和二肽重复蛋白(DPR)沉积,也可能与其他神经退行性相关蛋白聚集物有关。在此,我们介绍了一位 74 岁快速进展性痴呆患者中 C9orf72 突变与散发性克雅氏病(CJD)的独特组合。

方法

详细的神经病理学检查,包括几种蛋白病变的免疫组织化学检查。遗传分析通过重复引物聚合酶链反应(PCR)进行。此外,我们分析了其他 C9orf72 突变携带者的脑组织中朊蛋白(PrP)沉积,并筛选了其他 CJD 病例的小脑皮质中 p62/DPR 神经元包含物,以评估合并病变的频率。

结果

一位快速进展性神经功能恶化 8 个月的患者的死后脑检查证实了 CJD 的诊断。她在 PRNP 密码子 129 处存在缬氨酸纯合性。此外,还发现了额颞叶变性(FTLD)模式,伴有 TDP-43 蛋白聚集物和 p62+/C9RANT+阳性包含物,以及高度的阿尔茨海默病相关病理学(A3B3C3)。通过重复引物 PCR 证实了疑似 C9orf72 扩展突变。13 例 C9orf72 病例的筛查未发现病理性 PrP 聚集物,100 例 CJD 病例的筛查未发现其他 C9orf72 扩展突变携带者。

结论

同一患者中 C9orf72 扩展突变相关 FTLD 与散发性 CJD 的组合很少见。虽然这两种疾病的罕见性使这种偶然事件的可能性最大,但这两种神经退行性病变之间是否存在潜在联系值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f2d5/7898301/14eca00116de/ENE-28-1009-g001.jpg

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