Literature DB >> 17502470

Hereditary spastic paraplegia 3A associated with axonal neuropathy.

Neviana Ivanova1, Kristl G Claeys, Tine Deconinck, Ivan Litvinenko, Albena Jordanova, Michaela Auer-Grumbach, Jana Haberlova, Ann Löfgren, Gisele Smeyers, Eva Nelis, Rudy Mercelis, Barbara Plecko, Josef Priller, Josef Zámecník, Berten Ceulemans, Anne Kjersti Erichsen, Erik Björck, Garth Nicholson, Michael W Sereda, Pavel Seeman, Ivo Kremensky, Vanio Mitev, Peter De Jonghe.   

Abstract

OBJECTIVE: To study the frequency and distribution of mutations in SPG3A in a large cohort of patients with hereditary spastic paraplegia.
DESIGN: We screened a large cohort of 182 families and isolated cases with pure or complex hereditary spastic paraplegia phenotypes, which were negative for mutations in SPG4.
RESULTS: In 12 probands (6.6%), we identified 12 different SPG3A mutations (11 missense and 1 insertion/frameshift) of which 7 were novel and 3 were de novo. We found incomplete penetrance in 1 family (G482V). In most cases, SPG3A mutations were associated with an early age at onset (mean, 3 y); however, in 1 family (R495W mutation), symptoms started later (mean, 14 y) with clear intrafamilial variability (8-28 y). Six patients with an SPG3A mutation (F151S, Q191R, M408T, G469A, R495W) originating from 5 unrelated families presented with a complex form of hereditary spastic paraplegia associated with a neuropathy (17%). Our electrophysiological and pathological findings confirmed an axonal sensory-motor neuropathy. There was no correlation between the genotype and the presence of a neuropathy.
CONCLUSIONS: We conclude that mutations in SPG3A represent an important cause of patients in the overall hereditary spastic paraplegia population. SPG3A is more often associated with a neuropathy than previously assumed. Therefore, patients with a bipyramidal syndrome and a neuropathy should be screened for mutations in SPG3A.

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Year:  2007        PMID: 17502470     DOI: 10.1001/archneur.64.5.706

Source DB:  PubMed          Journal:  Arch Neurol        ISSN: 0003-9942


  15 in total

Review 1.  Recent advances in the genetics of spastic paraplegias.

Authors:  Giovanni Stevanin; Merle Ruberg; Alexis Brice
Journal:  Curr Neurol Neurosci Rep       Date:  2008-05       Impact factor: 5.081

2.  Extending the clinical spectrum of SPG3A mutations to a very severe and very early complicated phenotype.

Authors:  J Haberlová; K G Claeys; J Zámecník; P De Jonghe; P Seeman
Journal:  J Neurol       Date:  2008-04-30       Impact factor: 4.849

3.  Complex phenotype in an Italian family with a novel mutation in SPG3A.

Authors:  Maria Fulvia de Leva; Alessandro Filla; Chiara Criscuolo; Alessandra Tessa; Sabina Pappatà; Mario Quarantelli; Leonilda Bilo; Silvio Peluso; Antonella Antenora; Dario Longo; Filippo M Santorelli; Giuseppe De Michele
Journal:  J Neurol       Date:  2009-09-19       Impact factor: 4.849

4.  A hereditary spastic paraplegia-associated atlastin variant exhibits defective allosteric coupling in the catalytic core.

Authors:  John P O'Donnell; Laura J Byrnes; Richard B Cooley; Holger Sondermann
Journal:  J Biol Chem       Date:  2017-11-27       Impact factor: 5.157

5.  Structures of the atlastin GTPase provide insight into homotypic fusion of endoplasmic reticulum membranes.

Authors:  Xin Bian; Robin W Klemm; Tina Y Liu; Miao Zhang; Sha Sun; Xuewu Sui; Xinqi Liu; Tom A Rapoport; Junjie Hu
Journal:  Proc Natl Acad Sci U S A       Date:  2011-02-22       Impact factor: 11.205

6.  Lipid interaction of the C terminus and association of the transmembrane segments facilitate atlastin-mediated homotypic endoplasmic reticulum fusion.

Authors:  Tina Y Liu; Xin Bian; Sha Sun; Xiaoyu Hu; Robin W Klemm; William A Prinz; Tom A Rapoport; Junjie Hu
Journal:  Proc Natl Acad Sci U S A       Date:  2012-07-16       Impact factor: 11.205

7.  Targeted high-throughput sequencing identifies mutations in atlastin-1 as a cause of hereditary sensory neuropathy type I.

Authors:  Christian Guelly; Peng-Peng Zhu; Lea Leonardis; Lea Papić; Janez Zidar; Maria Schabhüttl; Heimo Strohmaier; Joachim Weis; Tim M Strom; Jonathan Baets; Jan Willems; Peter De Jonghe; Mary M Reilly; Eleonore Fröhlich; Martina Hatz; Slave Trajanoski; Thomas R Pieber; Andreas R Janecke; Craig Blackstone; Michaela Auer-Grumbach
Journal:  Am J Hum Genet       Date:  2010-12-30       Impact factor: 11.025

8.  Membrane fusion by the GTPase atlastin requires a conserved C-terminal cytoplasmic tail and dimerization through the middle domain.

Authors:  Tyler J Moss; Camilla Andreazza; Avani Verma; Andrea Daga; James A McNew
Journal:  Proc Natl Acad Sci U S A       Date:  2011-06-20       Impact factor: 11.205

9.  Inhibition of TFG function causes hereditary axon degeneration by impairing endoplasmic reticulum structure.

Authors:  Christian Beetz; Adam Johnson; Amber L Schuh; Seema Thakur; Rita-Eva Varga; Thomas Fothergill; Nicole Hertel; Ewa Bomba-Warczak; Holger Thiele; Gudrun Nürnberg; Janine Altmüller; Renu Saxena; Edwin R Chapman; Erik W Dent; Peter Nürnberg; Anjon Audhya
Journal:  Proc Natl Acad Sci U S A       Date:  2013-03-11       Impact factor: 11.205

Review 10.  Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular mechanisms.

Authors:  John K Fink
Journal:  Acta Neuropathol       Date:  2013-07-30       Impact factor: 17.088

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