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Article

Distinct TDP-43 pathology in ALS patients with ataxin 2 intermediate-length polyQ expansions

19 Apr 2012

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 22526021
DOI: 10.1007/s00401-012-0985-5

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Related research

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Distinct TDP-43 pathology in ALS patients with ataxin 2 intermediate-length polyQ expansionsPMID 22526021Read ↗

FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansionSemantic proximity Read ↗

Ataxin-2 polyQ expansions in FTLD-ALS spectrum disorders in Flanders-Belgian cohortsSemantic proximity Read ↗

ALS risk but not phenotype is affected by ataxin-2 intermediate length polyglutamine expansion.Semantic proximity Read ↗

Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS.Semantic proximity Read ↗

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Ataxin-2 polyglutamine expansions aberrantly sequester TDP-43 ribonucleoprotein condensates disrupting mRNA transport and local translation in neuronsSemantic proximity Read ↗

Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin‐2 to induce motor neuron dysfunction and cell deathSemantic proximity Read ↗

Ataxin-2 intermediate-length polyglutamine expansions in European ALS patientsSemantic proximity Read ↗

Model Organisms Reveal Insight into Human Neurodegenerative Disease: Ataxin-2 Intermediate-Length Polyglutamine Expansions Are a Risk Factor for ALSSemantic proximity Read ↗

Expanding the spectrum of annexin A11 proteinopathy in frontotemporal lobar degeneration and motor neuron diseaseSemantic proximity Read ↗

Molecular Dissection of TDP-43 ProteinopathiesSemantic proximity Read ↗

ATAXIN-2 intermediate-length polyglutamine expansions elicit ALS-associated metabolic and immune phenotypes.Semantic proximity Read ↗

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