| Literature DB >> 26751646 |
Shakeela Daud1, Naseebullah Kakar2,3,4, Ingrid Goebel2,5, Abu Saeed Hashmi1, Tahir Yaqub1,6, Gudrun Nürnberg7, Peter Nürnberg7,8,9, Deborah J Morris-Rosendahl10,11, Muhammad Wasim1, Alexander E Volk2,5, Christian Kubisch2,5, Jamil Ahmad4, Guntram Borck2.
Abstract
Biallelic mutations of ALS2 cause a clinical spectrum of overlapping autosomal recessive neurodegenerative disorders: infantile-onset ascending hereditary spastic paralysis (IAHSP), juvenile primary lateral sclerosis (JPLS), and juvenile amyotrophic lateral sclerosis (ALS2). We report on eleven individuals affected with IAHSP from two consanguineous Pakistani families. A combination of linkage analysis with homozygosity mapping and targeted sequencing identified two novel ALS2 mutations, a c.194T > C (p.Phe65Ser) missense substitution located in the first RCC-like domain of ALS2/alsin and a c.2998delA (p.Ile1000*) nonsense mutation. This study of extended families including a total of eleven affected individuals suggests that a given ALS2 mutation may lead to a phenotype with remarkable intrafamilial clinical homogeneity.Entities:
Keywords: ALS2; alsin; amyotrophic lateral sclerosis; infantile-onset ascending hereditary spastic paralysis (IAHSP)
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Year: 2016 PMID: 26751646 DOI: 10.3109/21678421.2015.1125501
Source DB: PubMed Journal: Amyotroph Lateral Scler Frontotemporal Degener ISSN: 2167-8421 Impact factor: 4.092