Institute of Neurogenetics, University of Lübeck, 23538, Lübeck, Germany.
Centogene AG, Rostock, Germany.
J Neurol. 2020 Mar;267(3):770-782. doi: 10.1007/s00415-019-09640-2. Epub 2019 Nov 20.
Neurometabolic disorders are often inherited and complex disorders that result from abnormalities of enzymes important for development and function of the nervous system. Recently, biallelic mutations in NAXE (APOA1BP) were found in patients with an infantile, lethal, neurometabolic disease. Here, exome sequencing was performed in two affected sisters and their healthy parents. The best candidate, NAXE, was tested for replication in exome sequencing data from 4351 patients with neurodevelopmental disorders. Quantitative RT-PCR, western blot and form factor analysis were performed to assess NAXE expression, protein levels and to analyze mitochondrial morphology in fibroblasts. Vitamin B3 was administered to one patient. Compound heterozygous missense (c.757G>A: p.Gly253Ser) and splicing (c.665-1G>A) variants in NAXE were identified in both affected sisters. In contrast to the previously reported patients with biallelic NAXE variants, our patients showed a milder phenotype with disease onset in early adulthood with psychosis, cognitive impairment, seizures, cerebellar ataxia and spasticity. The symptoms fluctuated. Additional screening of NAXE identified three novel homozygous missense variants (p.Lys245Gln, p.Asp218Asn, p.Ile214Val) in three patients with overlapping phenotype (fluctuating disease course, respiratory insufficiency, movement disorder). Lastly, patients with the c.665-1G>A splicing variant showed a significant reduction of NAXE expression compared to control fibroblasts and undetectable NAXE protein levels compared to control fibroblasts. Based on the metabolic pathway, vitamin B3 and coenzyme Q treatment was introduced in one patient in addition to antiepileptic treatment. This combination and avoidance of triggers was associated with continuous motor and cognitive improvement. The NAXE variants identified in this study suggest a loss-of-function mechanism leading to an insufficient NAD(P)HX repair system. Importantly, symptoms of patients with NAXE variants may improve with vitamin B3/coenzyme Q administration.
神经代谢障碍通常是由影响神经系统发育和功能的酶的异常引起的遗传和复杂疾病。最近,在患有婴儿期致死性神经代谢疾病的患者中发现了 NAXE(APOA1BP)的双等位基因突变。在此,对两名受影响的姐妹及其健康父母进行了外显子组测序。最佳候选基因 NAXE 在来自 4351 名神经发育障碍患者的外显子组测序数据中进行了复制测试。进行定量 RT-PCR、western blot 和形态因子分析以评估成纤维细胞中的 NAXE 表达、蛋白水平和分析线粒体形态。对一名患者给予维生素 B3 治疗。在两名受影响的姐妹中均发现了 NAXE 的复合杂合错义(c.757G>A:p.Gly253Ser)和剪接(c.665-1G>A)变体。与先前报道的具有双等位基因 NAXE 变体的患者不同,我们的患者表现出较轻的表型,疾病在成年早期发作,伴有精神病、认知障碍、癫痫发作、小脑共济失调和痉挛。症状波动。对 NAXE 的进一步筛选在具有重叠表型(病情波动、呼吸功能不全、运动障碍)的三名患者中发现了三个新的纯合错义变体(p.Lys245Gln、p.Asp218Asn、p.Ile214Val)。最后,与对照成纤维细胞相比,携带 c.665-1G>A 剪接变体的患者的 NAXE 表达显著降低,与对照成纤维细胞相比,无法检测到 NAXE 蛋白水平。基于代谢途径,除了抗癫痫治疗外,还向一名患者引入了维生素 B3 和辅酶 Q 治疗。这种组合和避免诱因与持续的运动和认知改善有关。本研究中鉴定的 NAXE 变体提示存在导致 NAD(P)HX 修复系统不足的功能丧失机制。重要的是,NAXE 变体患者的症状可能会随着维生素 B3/辅酶 Q 的给予而改善。