Evidence map›Paper›PMID 23358603›Full record

ArticleBrain : a journal of neurology2013

Corticospinal tract degeneration associated with TDP-43 type C pathology and semantic dementia.

Keith A Josephs, Jennifer L Whitwell, Melissa E Murray, Joseph E Parisi, Neill R Graff-Radford, David S Knopman, Bradley F Boeve, Matthew L Senjem, Rosa Rademakers, Clifford R Jack and 2 more

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in Brain : a journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
  6. Semantic variant primary progressive aphasia with ANXA11 p.D40G.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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  16. Correcting miR92a-vGAT-Mediated GABAergic Dysfunctions Rescues Human Tau-Induced Anxiety in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2017
    Article
  17. Article
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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

12 authors at 3 institutions in 1 country.

Keith A JosephsBehavioural Neurology, Department of Neurology, Mayo Clinic, Rochester, MN 55905, USA. josephs.keith@mayo.edu
Jennifer L Whitwell
Melissa E Murray
Joseph E Parisi
Neill R Graff-Radford
David S Knopman
Bradley F Boeve
Matthew L Senjem
Rosa Rademakers
Clifford R Jack
Ronald C Petersen
Dennis W Dickson
Mayo Clinic · USMayo Clinic in Florida · USMayo Clinic in Arizona · US

Funding

Vascular Structure and Function in Cognitive AgingP01AG003949 · NIA · YESHIVA UNIVERSITY · PI Richard B. LIPTON · 1985 to 2026
$73.9M
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
Understanding the role of TDP-43 in Alzheimers disease and FTLDR01AG037491 · NIA · MAYO CLINIC ROCHESTER · PI JOSEPHS, KEITH A · 2010 to 2024
$6.5M
NIA NIH HHS P01 AG003949NIA NIH HHS P01 AG03949NIA NIH HHS P50 AG016574NIA NIH HHS P50 AG16574NIA NIH HHS R01 AG037491NINDS NIH HHS P50 NS072187NINDS NIH HHS P50 NS72187
6 · The paper itself

Abstract

Four subtypes of frontotemporal lobar degeneration with TDP-43 immunoreactive inclusions have been described (types A-D). Of these four subtypes, motor neuron disease is more commonly associated with type B pathology, but has also been reported with type A pathology. We have noted, however, the unusual occurrence of cases of type C pathology having corticospinal tract degeneration. We aimed to assess the severity of corticospinal tract degeneration in a large cohort of cases with type C (n = 31). Pathological analysis included semi-quantitation of myelin loss of fibres of the corticospinal tract and associated macrophage burden, as well as axonal loss, at the level of the medullary pyramids. We also assessed for motor cortex degeneration and fibre loss of the medial lemniscus/olivocerebellar tract. All cases were subdivided into three groups based on the degree of corticospinal tract degeneration: (i) no corticospinal tract degeneration; (ii) equivocal corticospinal tract degeneration; and (iii) moderate to very severe corticospinal tract degeneration. Clinical, genetic, pathological and imaging comparisons were performed across groups. Eight cases had no corticospinal tract degeneration, and 14 cases had equivocal to mild corticospinal tract degeneration. Nine cases, however, had moderate to very severe corticospinal tract degeneration with myelin and axonal loss. In these nine cases, there was degeneration of the motor cortex without lower motor neuron degeneration or involvement of other brainstem tracts. These cases most commonly presented as semantic dementia, and they had longer disease duration (mean: 15.3 years) compared with the other two groups (10.8 and 9.9 years; P = 0.03). After adjusting for disease duration, severity of corticospinal tract degeneration remained significantly different across groups. Only one case, without corticospinal tract degeneration, was found to have a hexanucleotide repeat expansion in the C9ORF72 gene. All three groups were associated with anterior temporal lobe atrophy on MRI; however, the cases with moderate to severe corticospinal tract degeneration showed right-sided temporal lobe asymmetry and greater involvement of the right temporal lobe and superior motor cortices than the other groups. In contrast, the cases with no or equivocal corticospinal tract degeneration were more likely to show left-sided temporal lobe asymmetry. For comparison, the corticospinal tract was assessed in 86 type A and B cases, and only two cases showed evidence of corticospinal tract degeneration without lower motor neuron degeneration. These findings confirm that there exists a unique association between frontotemporal lobar degeneration with type C pathology and corticospinal tract degeneration, with this entity showing a predilection to involve the right temporal lobe.

Indexed as

DNA-Binding ProteinsAgedAged, 80 and overCohort StudiesFemaleFrontotemporal Lobar DegenerationHumansMaleMiddle AgedNerve DegenerationPyramidal TractsDNA-Binding Proteins

Identifiers

PMID23358603
PMCPMC3572926
OpenAlexW2161768758

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.