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由朊蛋白基因第 105 密码子脯氨酸到亮氨酸突变引起的格斯特曼-施特劳斯勒-谢因克病的区域性脑血流的连续变化。

Serial changes in regional cerebral blood flow in Gerstmann-Sträussler-Scheinker disease caused by a Pro-to-Leu mutation at codon 105 in the prion protein gene.

机构信息

Department of Neurology and Neurological Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, Japan.

出版信息

Prion. 2023 Dec;17(1):138-140. doi: 10.1080/19336896.2023.2256928.

Abstract

Gerstmann-Sträussler-Scheinker disease with a Pro-to-Leu substitution at codon 105 in the prion protein gene (GSS-P105L) is a rare variant of human genetic prion disease. Herein, we report the case of a patient with GSS-P105L, who showed serial changes in regional cerebral blood flow (rCBF) on single-photon emission computed tomography (SPECT). A 42-year-old woman, with an affected father presenting with similar symptoms, had a 1-year history of progressive gait disturbance, lower-limb spasticity, and psychiatric symptoms. Genetic analysis confirmed the diagnosis of GSS-P105L. Eleven months after disease onset, brain magnetic resonance imaging (MRI) showed bilateral frontal lobe-dominant cerebral atrophy without hyperintensity on diffusion-weighted imaging (DWI) sequences; meanwhile, SPECT revealed non-specific mild hypoperfusion. Follow-up MRI at 52 months after onset demonstrated progressive frontal lobe-dominant cerebral atrophy without hyperintensity on DWI, while SPECT revealed a marked decrease in rCBF in the bilateral right-dominant frontal lobe. Patients with GSS with a Pro-to-Leu substitution at codon 102 (GSS-P102L) have been reported to exhibit hyperintensity on DWI-MRI and a diffuse decrease in CBF with a mosaic-like pattern on SPECT, which is absent in patients with GSS-P105L, thereby possibly reflecting the differences in pathophysiology between GSS-P102L and GSS-P105L.

摘要

Gerstmann-Straussler-Scheinker 病伴朊蛋白基因第 105 密码子脯氨酸至亮氨酸替换(GSS-P105L)是一种罕见的人类遗传性朊病毒病变异型。在此,我们报告了一例 GSS-P105L 患者,其单光子发射计算机断层扫描(SPECT)显示区域性脑血流(rCBF)的连续变化。一位 42 岁的女性,其患病父亲表现出类似的症状,有 1 年的进行性步态障碍、下肢痉挛和精神症状病史。基因分析证实了 GSS-P105L 的诊断。疾病发病后 11 个月,脑磁共振成像(MRI)显示双侧额叶为主的脑萎缩,弥散加权成像(DWI)序列未见高信号;同时,SPECT 显示非特异性轻度低灌注。发病后 52 个月的随访 MRI 显示双侧额叶为主的脑进行性萎缩,DWI 序列未见高信号,而 SPECT 显示双侧右侧额叶 rCBF 明显减少。据报道,GSS 中第 102 密码子脯氨酸至亮氨酸替换(GSS-P102L)的患者在 DWI-MRI 上表现为高信号,SPECT 上表现为 CBF 弥漫性减少伴镶嵌样模式,而 GSS-P105L 患者则无此表现,这可能反映了 GSS-P102L 和 GSS-P105L 之间在发病机制上的差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f27e/10503442/42a5db9cb4dc/KPRN_A_2256928_F0001_OC.jpg

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