Department of Pediatric Neurology, Sütçü İmam Universty Faculty of Medicine, Kahramanmaraş, Turkey.
Department of Pediatric Neurology, Konya City Hospital, Konya, Turkey.
Clin Neurol Neurosurg. 2022 Dec;223:107509. doi: 10.1016/j.clineuro.2022.107509. Epub 2022 Nov 3.
Developmental and epileptic encephalopathies (DEEs) are heterogeneous severe neurodevelopmental disorders characterized by recurrent clinical seizures that begin in the neonatal period and early childhood and regression or delay in cognitive, sensory and motor skills in the context of accompanying epileptiform abnormalities. Adaptor-related protein complex 3 beta-2 subunit (AP3B2) gene variants are thought to cause disruption of neuron-specific neurotransmitter release.
In this case report, whole exome sequencing (WES) was performed on two of the four pediatric patients who came from two unrelated families and were affected by DEE. As a result of WES, previously unreported variants, that is, p.Ala149Serfs* 34 and p.Pro993Argfs* 5, were detected in the AP3B2 gene. These variants were studied using Sanger sequencing in the siblings affected by DEE of the said pediatric patients and in their healthy parents.
Autosomal recessive variants of the AP3B2 are associated with the development of DEE. To date, only 14 cases of AP3B2 mutations have been reported in the literature. Consequentially, DEE phenotype involving severe global developmental delay emerged, which is characterized by early-onset infantile epileptic encephalopathy, severe hypotonia, postnatal microcephaly, poor eye contact, speech retardation, abnormal involuntary movements, stereotypical hand movements, progressive intellectual disability, and behavioral and neuropsychiatric findings.
Given the limited number of patients reported in the literature, detailed studies of the specific clinical and molecular features of AP3B2 gene variants, will shed light on the genotype-phenotype correlation.
发育性和癫痫性脑病(DEE)是一种异质性严重神经发育障碍,其特征是新生儿期和幼儿期反复发作的临床癫痫发作,并伴有癫痫样异常,认知、感觉和运动技能出现退化或延迟。衔接蛋白相关 3β-2 亚基(AP3B2)基因突变被认为会导致神经元特异性神经递质释放中断。
本病例报告对来自两个无关家庭的 4 名儿科患者中的 2 名进行了全外显子组测序(WES)。由于 WES,在 AP3B2 基因中检测到了先前未报道的变异,即 p.Ala149Serfs34 和 p.Pro993Argfs5。在受影响的儿科患者的 DEE 兄弟姐妹及其健康父母中,使用 Sanger 测序研究了这些变体。
AP3B2 的常染色体隐性变体与 DEE 的发展有关。迄今为止,文献中仅报道了 14 例 AP3B2 突变病例。因此,出现了涉及严重全面发育迟缓的 DEE 表型,其特征为早发性婴儿癫痫性脑病、严重的肌张力低下、产后小头畸形、眼神交流不良、言语发育迟缓、异常不自主运动、刻板的手部运动、进行性智力障碍以及行为和神经精神学发现。
鉴于文献中报告的患者数量有限,对 AP3B2 基因突变的特定临床和分子特征进行详细研究,将有助于阐明基因型-表型相关性。