Evidence map›Paper›PMID 25917047›Full record

ArticleActa neuropathologica2015

A truncating SOD1 mutation, p.Gly141X, is associated with clinical and pathologic heterogeneity, including frontotemporal lobar degeneration.

Masataka Nakamura, Kevin F Bieniek, Wen-Lang Lin, Neill R Graff-Radford, Melissa E Murray, Monica Castanedes-Casey, Pamela Desaro, Matthew C Baker, Nicola J Rutherford, Janice Robertson and 3 more

Open access · greenAbstract readCase Reports
In one paragraph

Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. ALS-plus related clinical and genetic study from China.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Article
  4. Review
  5. Article
  6. Article
  7. Modelling amyotrophic lateral sclerosis in rodents.Nature reviews. Neuroscience · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Masataka NakamuraNeuropathology Laboratory, Department of Neuroscience, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL, 32224, USA.
Kevin F Bieniek
Wen-Lang Lin
Neill R Graff-Radford
Melissa E Murray
Monica Castanedes-Casey
Pamela Desaro
Matthew C Baker
Nicola J Rutherford
Janice Robertson
Rosa Rademakers
Dennis W Dickson
Kevin B Boylan
Mayo Clinic in Florida · USOccupational Cancer Research Centre · CAUniversity of Toronto · CA

Funding

THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI BU, GUOJUN · 1999 to 2018
$36.9M
Neuropathology CoreP50NS072187 · NINDS · MAYO CLINIC JACKSONVILLE · PI DICKSON, DENNIS WILLIAM · 2010 to 2017
$8.7M
The genetics of chromosome 17q21-linked tau-negative FTDR01AG026251 · NIA · MAYO CLINIC JACKSONVILLE · PI PETRUCELLI, LEONARD · 2006 to 2014
$1.9M
Progranulin: Mutation and Regulation in Neurodegenerative diseaseR01NS065782 · NINDS · MAYO CLINIC JACKSONVILLE · PI RADEMAKERS, ROSA · 2009 to 2012
$1.3M
NIA NIH HHS P50 AG016574NIA NIH HHS P50 AG16574NIA NIH HHS R01 AG026251NINDS NIH HHS P50 NS072187NINDS NIH HHS R01 NS065782
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a degenerative disorder affecting upper and lower motor neurons, but it is increasingly recognized to affect other systems, with cognitive impairment resembling frontotemporal dementia (FTD) in some patients. We report clinical and pathologic findings of a family with ALS due to a truncating mutation, p.Gly141X, in copper/zinc superoxide dismutase (SOD1). The proband presented clinically with FTD and later showed progressive motor neuron disease, while all other family members had early-onset and rapidly progressive ALS without significant cognitive deficits. Pathologic examination of both the proband and her daughter revealed degeneration of corticospinal tracts and motor neurons in brain and spinal cord compatible with ALS. On the other hand, the proband also had neocortical and limbic system degeneration with pleomorphic neuronal cytoplasmic inclusions. Extramotor pathology in her daughter was relatively restricted to the hypothalamus and extrapyramidal system, but not the neocortex. The inclusions in the proband and her daughter were immunoreactive for SOD1, but negative for TAR DNA-binding protein of 43 kDa (TDP-43). In the proband, a number of the neocortical inclusions were immunopositive for α-internexin, initially suggesting a diagnosis of atypical FTLD, but there was no evidence of fused in sarcoma (FUS) immunoreactivity, which is often detected in atypical FTLD. Analogous to atypical FTLD, neuronal inclusions had variable co-localization of SOD1 and α-internexin. The current classification of FTLD is based on the major constituent protein: FTLD-tau, FTLD-TDP-43, and FTLD-FUS. The proband in this family indicates that SOD1, while rare, can also be the substrate of FTLD, in addition to the more common presentation of ALS. The explanation for clinical and pathologic heterogeneity of SOD1 mutations, including the p.Gly141X mutation, remains unresolved.

Indexed as

MutationAdultAmyotrophic Lateral SclerosisBrainFamilyFatal OutcomeFemaleFrontotemporal Lobar DegenerationHumansMaleMiddle AgedPedigreeSuperoxide DismutaseSuperoxide Dismutase-1SOD1 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1

Identifiers

PMID25917047
PMCPMC5039014
OpenAlexW1990635190

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.