Evidence map›Paper›PMID 27220776›Full record

ArticleJournal of neuroinflammation2016

Inflammatory profile in LRRK2-associated prodromal and clinical PD.

Kathrin Brockmann, Anja Apel, Claudia Schulte, Nicole Schneiderhan-Marra, Claustre Pont-Sunyer, Dolores Vilas, Javier Ruiz-Martinez, Markus Langkamp, Jean-Christophe Corvol, Florence Cormier and 12 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 10% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Parkinson's-Linked LRRK2 and GBA1 Mutations Modulate the Peripheral Immune Response to Pseudomonas aeruginosa.Movement disorders : official journal of the Movement Disorder Society · 2026
    Article
  5. Article
  6. Article
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  8. Integrated Stress Response Signatures Drive Monocyte Dysfunction inmedRxiv : the preprint server for health sciences · 2025
    Article
  9. Brain communications · 2025
    Article
  10. Exploring LRRK2-dependent Mechanisms in Parkinson's Disease Therapy.CNS & neurological disorders drug targets · 2025
    Review
  11. Article
  12. LRRK2-Associated Parkinsonism With and WithoutmedRxiv : the preprint server for health sciences · 2024
    Article
  13. Review
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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

22 authors at 15 institutions in 6 countries.

Kathrin BrockmannDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany. Kathrin.Brockmann@uni-tuebingen.de.
Anja ApelDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Claudia SchulteDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Nicole Schneiderhan-MarraNatural and Medical Sciences Institute at the University of Tübingen (NMI), Reutlingen, Germany.
Claustre Pont-SunyerParkinson's Disease and Movement Disorders Unit, Neurology Service, Hospital Clinic de Barcelona, Universitat de Barcelona, Institutd'Investigacions Biomediques August Pi I Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Dolores VilasParkinson's Disease and Movement Disorders Unit, Neurology Service, Hospital Clinic de Barcelona, Universitat de Barcelona, Institutd'Investigacions Biomediques August Pi I Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Javier Ruiz-MartinezHospital Universitario Donostia, Biodonostia Institut, San Sebastián, Guipuzcoa, Spain.
Markus LangkampMediagnost GmbH, Reutlingen, Germany.
Jean-Christophe CorvolDépartement de Génétique et Cytogénétique, INSERM, Sorbonne Universités, Hôpital de la Pitié Salpêtrière, Paris, France.
Florence CormierDépartement de Génétique et Cytogénétique, INSERM, Sorbonne Universités, Hôpital de la Pitié Salpêtrière, Paris, France.
Thomas KnorppNatural and Medical Sciences Institute at the University of Tübingen (NMI), Reutlingen, Germany.
Thomas O JoosNatural and Medical Sciences Institute at the University of Tübingen (NMI), Reutlingen, Germany.
Thomas GasserDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Birgitt SchüleParkinson Institute and Clinical Center, 675 Almanor Ave, Sunnyvale, CA, USA.
Jan O AaslyDepartment of Neurology, St. Olavs Hospital, Trondheim, Norway.
Tatiana ForoudDepartment of Medical and Molecular Genetics, Indiana University, Bloomington, IN, USA.
Jose Felix Marti-MassoHospital Universitario Donostia, Biodonostia Institut, San Sebastián, Guipuzcoa, Spain.
Alexis BriceDépartement de Génétique et Cytogénétique, INSERM, Sorbonne Universités, Hôpital de la Pitié Salpêtrière, Paris, France.
Eduardo TolosaParkinson's Disease and Movement Disorders Unit, Neurology Service, Hospital Clinic de Barcelona, Universitat de Barcelona, Institutd'Investigacions Biomediques August Pi I Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Barcelona, Spain.
Connie MarrasMorton and Gloria Shulman Movement Disorders Centre and the Edmond J Safra Program in Parkinson's disease, Toronto Western Hospital, University of Toronto, Toronto, Canada.
Daniela BergDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
Walter MaetzlerDepartment of Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.
German Center for Neurodegenerative Diseases · DEUniversity of Tübingen · DEBiogipuzkoa Health Research Institute · ESHertie Institute for Clinical Brain Research · DEPitié-Salpêtrière Hospital · FRConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESHospital Clínic de Barcelona · ESImmundiagnostik (Germany) · DEIndiana University Bloomington · USNatural and Medical Sciences Institute · DEParkinson's Institute and Clinical Center · USSorbonne Université · FRSt Olav's University Hospital · NOToronto Western Hospital · CAUniversitat de Barcelona · ES

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
NCATS NIH HHS UL1 TR001108
6 · The paper itself

Abstract

backgroundThere is evidence for a relevant role of inflammation in the pathogenesis of Parkinson's disease (PD). Mutations in the LRRK2 gene represent the most frequent genetic cause for autosomal dominant PD. LRRK2 is highly expressed in macrophages and microglia suggesting an involvement in inflammatory pathways. The objectives are to test (1) whether idiopathic PD and LRRK2-associated PD share common inflammatory pathways or present distinct profiles and (2) whether non-manifesting LRRK2 mutation carriers present with similar aspects of inflammatory profiles as seen in PD-affected patients.

methodsWe assessed serum profiles of 23 immune-associated markers and the brain-derived neurotrophic factor in 534 individuals from the MJFF LRRK2 consortium.

resultsA large proportion of inflammatory markers were gender-dependent. Both PD-affected cohorts showed increased levels of the pro-inflammatory marker fatty-acid-binding protein. Additionally, idiopathic PD but not LRRK2-associated PD patients showed increased levels of the pro-inflammatory marker interleukin-12-p40 as well as the anti-inflammatory species interleukin-10, brain-derived neurotrophic factor, and stem cell factor. Non-manifesting LRRK2 mutation carriers including those with prodromal characteristics of PD presented with control-like inflammatory profiles.

conclusionsConcomitant inflammation seems to be associated with idiopathic and LRRK2-associated PD. Identifying PD patients in whom inflammatory processes play a major role in their pathophysiology might offer a new therapeutic window at least for a subgroup of patients. Since non-manifesting LRRK2 mutation carriers with symptoms of the prodromal phase of PD did not show inflammatory profiles, activation of the immune system seems not an early event in the disease cascade.

Indexed as

AdolescentAdultAgedAged, 80 and overBiocompatible MaterialsCohort StudiesCytokinesFemaleGene Expression RegulationHumansIntercellular Adhesion Molecule-1Interleukin-10Interleukin-12International CooperationLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Linear ModelsBiocompatible MaterialsCytokinesIntercellular Adhesion Molecule-1Interleukin-10Interleukin-12Leucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanImmuneInflammationLRRK2Parkinson

Identifiers

PMID27220776
PMCPMC4879729
OpenAlexW2394851933

What OpenQuestion holds

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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.