Evidence map›Paper›PMID 41623670›Full record

ArticleBrain, behavior, & immunity - health2026

Systemic inflammation and its associations in acute moderate-severe Traumatic Brain Injury: a cross-sectional study.

Lucia M Li, Eleftheria Kodosaki, Chloe J Y Xu, Amanda Heslegrave, Henrik Zetterberg, Neil S N Graham, Karl A Zimmerman, Elena Garbero, Federico Moro, Sandra Magnoni and 3 more

Abstract read
In one paragraph

Article in Brain, behavior, & immunity - health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

13 authors.

Lucia M LiDepartment of Brain Sciences, Imperial College London, Sir Michael Uren Building, 86 Wood Lane, W12 0BZ, UK.
Eleftheria KodosakiDepartment of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.
Chloe J Y XuDepartment of Brain Sciences, Imperial College London, Sir Michael Uren Building, 86 Wood Lane, W12 0BZ, UK.
Amanda HeslegraveDepartment of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.
Henrik ZetterbergDepartment of Neurodegenerative Disease, UCL Institute of Neurology, London, UK.
Neil S N GrahamDepartment of Brain Sciences, Imperial College London, Sir Michael Uren Building, 86 Wood Lane, W12 0BZ, UK.
Karl A ZimmermanDepartment of Brain Sciences, Imperial College London, Sir Michael Uren Building, 86 Wood Lane, W12 0BZ, UK.
Elena GarberoDepartment of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Federico MoroDepartment of Acute Brain and Cardiovascular Injury, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Sandra MagnoniDepartment of Medicine, Surgery and Pharmacy, University of Sassari, Sassari, Italy.
Guido BertoliniDepartment of Medical Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
David J LoaneSchool of Biochemistry and Immunology, Trinity College Dublin, Ireland.
David J SharpDepartment of Brain Sciences, Imperial College London, Sir Michael Uren Building, 86 Wood Lane, W12 0BZ, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic Brain Injury (TBI) triggers an acute systemic inflammatory response, which may impact outcomes. This response may interact with pre-existing factors linked to inflammation, such as age, to influence outcomes. Previous studies have typically measured few cytokines, but high-dimensional proteomic approaches can sensitively detect a broad range of inflammatory markers, to better characterise post-TBI inflammation. We analysed plasma from BIO-AX-TBI study participants (n = 37 acute moderate-severe TBI (Mayo Criteria), n = 22 acute non-TBI trauma (NTT), n = 28 non-injured controls (CON)) using the Alamar NULISA™ panel (>200 inflammatory markers). The NTT group enabled differentiation of TBI-specific versus general injury-related responses. Inflammatory markers were correlated with plasma NFL, GFAP, total tau, UCH-L1 (Simoa®), S100B (Millipore), and subacute (10 days-6 weeks) 3T MRI measures of lesion volume and white matter injury. Differential expression analysis identified four markers elevated specifically in TBI (VSNL1, IL1RN/IL-1Ra, GFAP, IKBKG), while other derangements reflected non-specific injury responses. Higher VSNL1 correlated with greater lesion volume (r

Indexed as

InflammationMRITraumatic brain injury

Identifiers

PMID41623670
PMCPMC12854048

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.