Donald Aimee, Tan Chong Y, Chakrapani Anupam, Hughes Derralyn A, Sharma Reena, Cole Duncan, Bardins Stanislav, Gorges Martin, Jones Simon A, Schneider Erich
Manchester Centre for Genomic Medicine, St Mary's Hospital, Manchester, UK.
Addenbrooke's Hospital, Cambridge, UK.
Orphanet J Rare Dis. 2020 Dec 17;15(1):349. doi: 10.1186/s13023-020-01637-9.
Neurological forms of Gaucher disease, the inherited disorder of β-Glucosylceramidase caused by bi-allelic variants in GBA1, is a progressive disorder which lacks a disease-modifying therapy. Systemic manifestations of disease are effectively treated with enzyme replacement therapy, however, molecules which cross the blood-brain barrier are still under investigation. Clinical trials of such therapeutics require robust, reproducible clinical endpoints to demonstrate efficacy and clear phenotypic definitions to identify suitable patients for inclusion in trials. The single consistent clinical feature in all patients with neuronopathic disease is the presence of a supranuclear saccadic gaze palsy, in the presence of Gaucher disease this finding serves as diagnostic of 'type 3' Gaucher disease.
We undertook a study to evaluate saccadic eye movements in Gaucher patients and to assess the role of the EyeSeeCam in measuring saccades. The EyeSeeCam is a video-oculography device which was used to run a protocol of saccade measures. We studied 39 patients with non-neurological Gaucher disease (type 1), 21 patients with type 3 (neurological) disease and a series of 35 healthy controls. Mean saccade parameters were compared across disease subgroups.
We confirmed the saccadic abnormality in patients with type 3 Gaucher disease and identified an unexpected subgroup of patients with type 1 Gaucher disease who demonstrated significant saccade parameter abnormalities. These patients also showed subtle neurological findings and shared a GBA1 variant.
This striking novel finding of a potentially attenuated type 3 Gaucher phenotype associated with a specific GBA1 variant and detectable saccadic abnormality prompts review of current disease classification. Further, this finding highlights the broad spectrum of neuronopathic Gaucher phenotypes relevant when designing inclusion criteria for clinical trials.
戈谢病的神经学形式是一种由GBA1基因双等位基因变异引起的β-葡萄糖神经酰胺酶遗传性疾病,是一种缺乏疾病修饰疗法的进行性疾病。该疾病的全身表现可通过酶替代疗法有效治疗,然而,能够穿过血脑屏障的分子仍在研究中。此类疗法的临床试验需要可靠、可重复的临床终点来证明疗效,以及清晰的表型定义来确定适合纳入试验的患者。所有患有神经病变疾病的患者唯一一致的临床特征是存在核上性扫视性凝视麻痹,在戈谢病患者中,这一发现可作为“3型”戈谢病的诊断依据。
我们开展了一项研究,以评估戈谢病患者的扫视眼动,并评估EyeSeeCam在测量扫视中的作用。EyeSeeCam是一种视频眼动描记设备,用于执行扫视测量方案。我们研究了39例非神经病变型戈谢病(1型)患者、21例3型(神经病变型)疾病患者以及35名健康对照者。比较了各疾病亚组的平均扫视参数。
我们证实了3型戈谢病患者存在扫视异常,并发现了1型戈谢病患者中的一个意外亚组,这些患者表现出明显的扫视参数异常。这些患者还表现出细微的神经学发现,并共享一个GBA1变异。
这一与特定GBA1变异相关且可检测到扫视异常的潜在弱化3型戈谢病表型的惊人新发现促使对当前疾病分类进行重新审视。此外,这一发现突出了在设计临床试验纳入标准时相关的神经病变型戈谢病表型的广泛范围。