Literature DB >> 30100179

Progressive cerebello-cerebral atrophy and progressive encephalopathy with edema, hypsarrhythmia and optic atrophy may be allelic syndromes.

Ronen Hady-Cohen1, Hila Ben-Pazi2, Vardit Adir3, Keren Yosovich4, Luba Blumkin5, Tally Lerman-Sagie5, Dorit Lev6.   

Abstract

In 2003, a new syndrome was described in the Sephardi Jewish population, named progressive cerebello-cerebral atrophy (PCCA) based on the typical neuroradiological findings. Following the identification of the causal genes in 2010 and 2014, two types were defined: PCCA type 1 due to SEPSECS mutations and PCCA type 2 due to VPS53 mutations. Progressive encephalopathy with edema, hypsarrhythmia and optic atrophy (PEHO) was described in 1991 in Finland. The clinical and radiological phenotype resembles PCCA. The genetic background has been elusive for many years. Recently, mutations in multiple genes including SEPSECS have been described in patients with a PEHO-like syndrome. In 2007 two siblings of Moroccan-Jewish origin were diagnosed as having PEHO due to a severe developmental encephalopathy, limb and facial edema, intractable epilepsy, optic atrophy in one sibling and dysmorphic features. Six years ago an extensive workup, including whole exome sequencing, did not reveal the cause. Recently, a clinical reevaluation of the siblings suggested the possibility that they suffer from PCCA. A reanalysis of the exome data from 2014 revealed that the siblings indeed carried the two VPS53 mutations (exon 19 c.2084A>G p.(Gln695Arg) and c.1556 + 5G>A) and the parents were found to be carriers. The discovery that mutations in both VPS53 and SEPSECS can present with a PEHO-like phenotype, place PCCA and PEHO on the same clinical spectrum and suggest they may be allelic syndromes.
Copyright © 2018 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Cerebellar atrophy; PCCA1; PCCA2; PEHO; SEPSECS; VPS53

Mesh:

Substances:

Year:  2018        PMID: 30100179     DOI: 10.1016/j.ejpn.2018.07.003

Source DB:  PubMed          Journal:  Eur J Paediatr Neurol        ISSN: 1090-3798            Impact factor:   3.140


  6 in total

1.  A neurodevelopmental disorder caused by mutations in the VPS51 subunit of the GARP and EARP complexes.

Authors:  David C Gershlick; Morié Ishida; Julie R Jones; Allison Bellomo; Juan S Bonifacino; David B Everman
Journal:  Hum Mol Genet       Date:  2019-05-01       Impact factor: 6.150

2.  ARFRP1 functions upstream of ARL1 and ARL5 to coordinate recruitment of distinct tethering factors to the trans-Golgi network.

Authors:  Morié Ishida; Juan S Bonifacino
Journal:  J Cell Biol       Date:  2019-10-01       Impact factor: 10.539

Review 3.  Membrane trafficking in health and disease.

Authors:  Rebecca Yarwood; John Hellicar; Philip G Woodman; Martin Lowe
Journal:  Dis Model Mech       Date:  2020-04-30       Impact factor: 5.758

4.  Case Report: A Relatively Mild Phenotype Produced by Novel Mutations in the SEPSECS Gene.

Authors:  Tingyu Rong; Ruen Yao; Yujiao Deng; Qingmin Lin; Guanghai Wang; Jian Wang; Fan Jiang; Yanrui Jiang
Journal:  Front Pediatr       Date:  2022-01-26       Impact factor: 3.418

5.  The GARP complex prevents sterol accumulation at the trans-Golgi network during dendrite remodeling.

Authors:  Caitlin E O'Brien; Susan H Younger; Lily Yeh Jan; Yuh Nung Jan
Journal:  J Cell Biol       Date:  2022-10-14       Impact factor: 8.077

6.  The Golgi-associated retrograde protein (GARP) complex plays an essential role in the maintenance of the Golgi glycosylation machinery.

Authors:  Amrita Khakurel; Tetyana Kudlyk; Juan S Bonifacino; Vladimir V Lupashin
Journal:  Mol Biol Cell       Date:  2021-06-23       Impact factor: 4.138

  6 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.