Evidence map›Paper›PMID 23718879›Full record

ArticleBMC neurology2013

Cerebrospinal fluid neurofilament light chain protein levels in subtypes of frontotemporal dementia.

Maria Landqvist Waldö, Alexander Frizell Santillo, Ulla Passant, Henrik Zetterberg, Lars Rosengren, Christer Nilsson, Elisabet Englund

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
7.4field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 128 citations in OpenAlex.

  1. Pooled it
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  12. Article
  13. Article
  14. Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Review
  17. Update on Major Neurocognitive Disorders.Focus (American Psychiatric Publishing) · 2021
    Article
  18. Article
  19. Fluid Biomarkers of Frontotemporal Lobar Degeneration.Advances in experimental medicine and biology · 2021
    Article
  20. Review

9 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Maria Landqvist WaldöSection of Geriatric Psychiatry, Department of Clinical Sciences, Lund University Hospital, Klinikgatan 22, Lund SE-221 85, Sweden. maria.landqvist@med.lu.se
Alexander Frizell Santillo
Ulla Passant
Henrik Zetterberg
Lars Rosengren
Christer Nilsson
Elisabet Englund
Lund University · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFrontotemporal dementia (FTD) is recognised as a clinically and morphologically heterogeneous group of interrelated neurodegenerative conditions. One of the subtypes within this disease spectrum is the behavioural variant FTD (bvFTD). This is known to be a varied disorder with a mixture of tau-positive and tau-negative underlying pathologies. The other subtypes include semantic dementia (SD), which generally exhibits tau-negative pathology, and progressive non-fluent aphasia (PNFA), which is usually tau-positive. As the clinical presentation of these subtypes may overlap, a specific diagnosis can be difficult to attain and today no specific biomarker can predict the underlying pathology. Neurofilament light chain protein (NFL), a cytoskeletal constituent of intermediate filaments, is thought to reflect neuronal and axonal death when appearing in the cerebrospinal fluid (CSF). NFL has been shown to be elevated in CSF in patients with FTD compared with AD and controls. Our hypothesis was that the levels of NFL also differ between the subtypes of FTD and may indicate the underlying pathological subtype.

methodsWe retrospectively analysed data from previous CSF analyses in 34 FTD cases (23 bvFTD, seven SD, four PNFA), 20 AD cases, and 26 healthy controls. A separate group of 10 neuropathologically verified and subtyped FTD cases (seven tau-negative, three tau-positive) were also analysed.

resultNFL levels were significantly higher in FTD compared with both AD (p<0.001) and controls (p<0.001). The NFL levels of SD and bvFTD were significantly higher (p<0.001) compared with AD. The biomarker profiles of PNFA and AD were similar. In the neuropathologically verified FTD cases, NFL was higher in the tau-negative than in the tau-positive cases (exact p=0.017).

conclusionsThe marked NFL elevation in some but not all FTD cases is likely to reflect the different underlying pathologies. The highest NFL values found in the SD group as well as in the neuropathologically verified tau-negative cases may be of subtype diagnostic value, if corroborated in larger patient cohorts. In bvFTD, a mixture of tau-positive and tau-negative underlying pathologies could possibly explain the intermediate NFL values.

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBrainCase-Control StudiesFemaleFrontotemporal DementiaHumansMaleMiddle AgedNeurofilament ProteinsNeurologic ExaminationPeptide FragmentsRetrospective StudiesAmyloid beta-Peptidesamyloid beta-protein (1-42)neurofilament protein LNeurofilament ProteinsPeptide Fragmentstau Proteins

Identifiers

PMID23718879
PMCPMC3671150
OpenAlexW2141909536

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.