Evidence map›Paper›PMID 37435933›Full record

ArticleBrain : a journal of neurology2023

Peripherin is a biomarker of axonal damage in peripheral nervous system disease.

Stephen Keddie, Duncan Smyth, Ryan Y S Keh, Michael K L Chou, Donna Grant, Sunaina Surana, Amanda Heslegrave, Henrik Zetterberg, Luuk Wieske, Milou Michael and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
13.0field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Observational
  7. The neuropathy-causingbioRxiv : the preprint server for biology · 2026
    Article
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  17. What is refractory CIDP?BMJ neurology open · 2026
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 4 countries.

Stephen KeddieDepartment of Neuromuscular Diseases, Barts Health NHS Trust, London E1 1BB, UK.ORCID 0000-0002-2102-6053
Duncan SmythDepartment of Neuromuscular Diseases, University College London, London WC1N 3BG, UK.
Ryan Y S KehDepartment of Neuromuscular Diseases, University College London, London WC1N 3BG, UK.ORCID 0000-0001-6434-9496
Michael K L ChouDepartment of Neuromuscular Diseases, University College London, London WC1N 3BG, UK.ORCID 0000-0003-3174-6027
Donna GrantNHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, London WC1N 3BG, UK.
Sunaina SuranaDepartment of Neuromuscular Diseases, University College London, London WC1N 3BG, UK.
Amanda HeslegraveUK Dementia Research Institute, University College London, London WC1E 6BT, UK.
Henrik ZetterbergUK Dementia Research Institute, University College London, London WC1E 6BT, UK.
Luuk WieskeDepartment of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands.ORCID 0000-0002-2522-4081
Milou MichaelDepartment of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands.
Filip EftimovDepartment of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands.
Roberto BellantiNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Simon RinaldiNuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.
Melanie S HartNHS Neuroimmunology and CSF Laboratory, Queen Square Institute of Neurology, London WC1N 3BG, UK.
Axel PetzoldDepartment of Neurology and Neurophysiology, Amsterdam Neuroscience, Amsterdam UMC, Location AMC, University of Amsterdam, 1081 HV Amsterdam, The Netherlands.ORCID 0000-0002-0344-9749
Michael P LunnDepartment of Neuromuscular Diseases, University College London, London WC1N 3BG, UK.
National Hospital for Neurology and Neurosurgery · GBAmsterdam Neuroscience · NLUniversity of Oxford · GBBarts Health NHS Trust · GBUK Dementia Research Institute · GBUniversity College London · GBUniversity of Wisconsin–Madison · US

Funding

Department of HealthMedical Research Council MR/X003922/1Medical Research Council MR/Y001826/1
6 · The paper itself

Abstract

Valid, responsive blood biomarkers specific to peripheral nerve damage would improve management of peripheral nervous system (PNS) diseases. Neurofilament light chain (NfL) is sensitive for detecting axonal pathology but is not specific to PNS damage, as it is expressed throughout the PNS and CNS. Peripherin, another intermediate filament protein, is almost exclusively expressed in peripheral nerve axons. We postulated that peripherin would be a promising blood biomarker of PNS axonal damage. We demonstrated that peripherin is distributed in sciatic nerve, and to a lesser extent spinal cord tissue lysates, but not in brain or extra-neural tissues. In the spinal cord, anti-peripherin antibody bound only to the primary cells of the periphery (anterior horn cells, motor axons and primary afferent sensory axons). In vitro models of antibody-mediated axonal and demyelinating nerve injury showed marked elevation of peripherin levels only in axonal damage and only a minimal rise in demyelination. We developed an immunoassay using single molecule array technology for the detection of serum peripherin as a biomarker for PNS axonal damage. We examined longitudinal serum peripherin and NfL concentrations in individuals with Guillain-Barré syndrome (GBS, n = 45, 179 time points), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, n = 35, 70 time points), multiple sclerosis (n = 30), dementia (as non-inflammatory CNS controls, n = 30) and healthy individuals (n = 24). Peak peripherin levels were higher in GBS than all other groups (median 18.75 pg/ml versus < 6.98 pg/ml, P < 0.0001). Peak NfL was highest in GBS (median 220.8 pg/ml) and lowest in healthy controls (median 5.6 pg/ml), but NfL did not distinguish between CIDP (17.3 pg/ml), multiple sclerosis (21.5 pg/ml) and dementia (29.9 pg/ml). While peak NfL levels were higher with older age (rho = +0.39, P < 0.0001), peak peripherin levels did not vary with age. In GBS, local regression analysis of serial peripherin in the majority of individuals with three or more time points of data (16/25) displayed a rise-and-fall pattern with the highest value within the first week of initial assessment. Similar analysis of serial NfL concentrations showed a later peak at 16 days. Group analysis of serum peripherin and NfL levels in GBS and CIDP patients were not significantly associated with clinical data, but in some individuals with GBS, peripherin levels appeared to better reflect clinical outcome measure improvement. Serum peripherin is a promising new, dynamic and specific biomarker of acute PNS axonal damage.

Indexed as

DementiaGuillain-Barre SyndromeMultiple SclerosisPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingAxonsBiomarkersHumansIntermediate FilamentsPeripherinsBiomarkersPeripherinsaxonbiomarkerguillain-Barré syndromeneuropathyperipheral nervous systemperipherin

Identifiers

PMID37435933
PMCPMC10629771
OpenAlexW4383980388

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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.