Evidence map›Paper›PMID 26410752›Full record

ArticleJournal of neurology2015

Dissecting IWG-2 typical and atypical Alzheimer's disease: insights from cerebrospinal fluid analysis.

Ross W Paterson, Jamie Toombs, Catherine F Slattery, Jennifer M Nicholas, Ulf Andreasson, Nadia K Magdalinou, Kaj Blennow, Jason D Warren, Cath J Mummery, Martin N Rossor and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Italian intersocietal recommendations for restructuring the diagnostic-therapeutic pathway for the implementation and appropriate use of anti-amyloid monoclonal antibodies in Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  4. Review
  5. International journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Diagnosis and Management of Posterior Cortical Atrophy.Current treatment options in neurology · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Aducanumab: Appropriate Use Recommendations.The journal of prevention of Alzheimer's disease · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

15 authors at 6 institutions in 2 countries.

Ross W PatersonDementia Research Centre, UCL Institute of Neurology, London, UK. r.paterson@ucl.ac.uk.
Jamie ToombsDepartment of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Catherine F SlatteryReta Lila Weston Institute, UCL Institute of Neurology, London, UK.
Jennifer M NicholasDepartment of Medical Statistics, London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT, UK.
Ulf AndreassonClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Nadia K MagdalinouReta Lila Weston Institute, UCL Institute of Neurology, London, UK.
Kaj BlennowClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Jason D WarrenDementia Research Centre, UCL Institute of Neurology, London, UK.
Cath J MummeryDementia Research Centre, UCL Institute of Neurology, London, UK.
Martin N RossorDementia Research Centre, UCL Institute of Neurology, London, UK.
Michael P LunnDepartment of Clinical Neuroimmunology, National Hospital for Neurology and Neurosurgery, London, UK.
Sebastian J CrutchDementia Research Centre, UCL Institute of Neurology, London, UK.
Nick C FoxDementia Research Centre, UCL Institute of Neurology, London, UK.
Henrik ZetterbergDepartment of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Jonathan M SchottDementia Research Centre, UCL Institute of Neurology, London, UK. j.schott@ucl.ac.uk.
University College London · GBUK Dementia Research Institute · GBNational Hospital for Neurology and Neurosurgery · GBUniversity of Gothenburg · SELondon School of Hygiene & Tropical Medicine · GBSahlgrenska University Hospital · SE

Funding

Medical Research Council MR/K000608/1
6 · The paper itself

Abstract

Pathobiological factors underlying phenotypic diversity in Alzheimer's disease (AD) are incompletely understood. We used an extended cerebrospinal fluid (CSF) panel to explore differences between "typical" with "atypical" AD and between amnestic, posterior cortical atrophy, logopenic aphasia and frontal variants. We included 97 subjects fulfilling International Working Group-2 research criteria for AD of whom 61 had "typical" AD and 36 "atypical" syndromes, and 30 controls. CSF biomarkers included total tau (T-tau), phosphorylated tau (P-tau), amyloid β1-42, amyloid βX-38/40/42, YKL-40, neurofilament light (NFL), and amyloid precursor proteins α and β. The typical and atypical groups were matched for age, sex, severity and rate of cognitive decline and had similar biomarker profiles, with the exception of NFL which was higher in the atypical group (p = 0.03). Sub-classifying the atypical group into its constituent clinical syndromes, posterior cortical atrophy was associated with the lowest T-tau [604.4 (436.8-675.8) pg/mL], P-tau (79.8 ± 21.8 pg/L), T-tau/Aβ1-42 ratio [2.3 (1.4-2.6)], AβX-40/X-42 ratio (22.1 ± 5.8) and rate of cognitive decline [1.9 (0.75-4.25) MMSE points/year]. Conversely, the frontal variant group had the highest levels of T-tau [1185.4 (591.7-1329.3) pg/mL], P-tau (116.4 ± 45.4 pg/L), T-tau/Aβ1-42 ratio [5.2 (3.3-6.9)] and AβX-40/X-42 ratio (27.9 ± 7.5), and rate of cognitive decline. Whilst on a group level IWG-2 "typical" and "atypical" AD share similar CSF profiles, which are very different from controls, atypical AD is a heterogeneous entity with evidence for subtle differences in amyloid processing and neurodegeneration between different clinical syndromes. These findings also have practical implications for the interpretation of clinical CSF biomarker results.

Indexed as

AgedAlzheimer DiseaseBiomarkersFemaleHumansMaleMiddle AgedBiomarkersAlzheimer’s diseaseBiomarkersCerebrospinal fluidIWG-2

Identifiers

PMID26410752
OpenAlexW1791696956

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.