Literature DB >> 23143971

Very mild presentation in adult with classical cellular phenotype of ataxia telangiectasia.

Paul F Worth1, Venkataramanan Srinivasan, Anna Smith, James I Last, Laura L Wootton, Paul M Biggs, Nicholas P Davies, Ellen F Carney, Philip J Byrd, A Malcolm R Taylor.   

Abstract

BACKGROUND: The major clinical feature of ataxia telangiectasia (A-T) is severe progressive neurodegeneration with onset in infancy. This classical A-T phenotype is caused by biallelic null mutations in the ATM gene, leading to the absence of ATM protein and increased cellular radiosensitivity. We report an unusual case of A-T in a 41-year-old mother, A-T210, who had very mild neurological symptoms despite complete loss of ATM protein.
METHODS: A neurological examination was performed, cellular radiosensitivity was assessed, and the ATM gene was sequenced. Skin fibroblasts and a lymphoblastoid cell line (LCL) were assayed for ATM protein expression and kinase activity.
RESULTS: Patient A-T210 showed mild chorea, dystonia, and gait ataxia, walked independently, and drove a car. LCL and skin fibroblasts were radiosensitive and did not express ATM protein. Two ATM-null mutations were identified.
CONCLUSIONS: The severe neurodegeneration resulting from loss of ATM can be mitigated in some circumstances.
Copyright © 2012 Movement Disorders Society.

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Year:  2012        PMID: 23143971     DOI: 10.1002/mds.25236

Source DB:  PubMed          Journal:  Mov Disord        ISSN: 0885-3185            Impact factor:   10.338


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