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Article

Increased incidence of the Hfe mutation in amyotrophic lateral sclerosis and related cellular consequences.

Journal of the neurological sciences - 15 Dec 2004

Wang Xin-Sheng, Lee Sang, Simmons Zachary, Boyer Philip, Scott Kevin, Liu Wenlei, Connor James

Abstract excerpt

The etiology of amyotrophic lateral sclerosis (ALS) is unknown. The presence of mutations in the superoxide dismutase gene (SOD1) has led to theories regarding a role for oxidative stress in the pathogenesis of this disease. A primary cause of oxidative stress is perturbations in cellular iron homeostasis. Cellular iron mismanagement and oxidative stress are associated with a number of neurodegenerative diseases....

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Source

Identifiers

PMID: 15546588
DOI: 10.1016/j.jns.2004.08.003

Genes

SOD1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Increased incidence of the Hfe mutation in amyotrophic lateral sclerosis and related cellular consequences.PMID 15546588Read ↗

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Consequences of expressing mutants of the hemochromatosis gene (HFE) into a human neuronal cell line lacking endogenous HFE.Semantic proximity Read ↗

HFE mutations and Alzheimer's diseaseSemantic proximity Read ↗

Misregulation of iron homeostasis in amyotrophic lateral sclerosis.Semantic proximity Read ↗

H63D HFE polymorphisms are associated with increased disease duration and decreased muscle superoxide dismutase-1 expression in amyotrophic lateral sclerosis patients.Semantic proximity Read ↗

H63D HFE genotype accelerates disease progression in animal models of amyotrophic lateral sclerosis.Semantic proximity Read ↗

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Expression of the HFE allelic variant H63D in SH-SY5Y cells affects tau phosphorylation at serine residues.Semantic proximity Read ↗

Manganese superoxide dismutase levels are elevated in a proportion of amyotrophic lateral sclerosis patient cell lines.Semantic proximity Read ↗

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