Evidence map›Paper›PMID 31542723›Full record

ReviewJournal of neurology, neurosurgery, and psychiatry2019

Understanding neurodegeneration after traumatic brain injury: from mechanisms to clinical trials in dementia.

Neil Sn Graham, David J Sharp

Registry-linked trialOpen access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neurology, neurosurgery, and psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05850000 (Dementia Clinical Trials), which is not on this map. Cited by 192 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 10 pooled it
20.8field-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.

NCT05850000 unknown statusnot on this mapstarted 2024, after this paper: background citation

Dementia Clinical Trials: A Study on the Clinical Trial Participation of Dementia Patients

TypeobservationalSponsorPower Life Sciences Inc.Ran2024 to 2026Enrolled500ConditionsDementia
3 · Its place in the literature

Who cites it

192 citing papers in PubMed, 10 syntheses or guidelines pooled it, 329 citations in OpenAlex.

  1. Practical Brain MRI Guidelines for Anti-Aβ Antibody Treatment in Early Symptomatic Alzheimer's Disease.Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine · 2025
    Guideline
  2. Guideline
  3. Pooled it
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  6. Glymphatic System a Window on TBI Pathophysiology: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  7. Pooled it
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  11. Trial
  12. Incidence and risk factors for AD/ADRD among American Indian and Alaska Native US Veterans.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  14. Article
  15. Article
  16. Observational
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132 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

2 authors at 2 institutions in 1 country.

Neil Sn GrahamBrain Sciences, Imperial College London, London, UK.ORCID 0000-0002-0183-3368
David J SharpBrain Sciences, Imperial College London, London, UK david.sharp@imperial.ac.uk.ORCID 0000-0003-4995-2240
Royal British Legion · GBUK Dementia Research Institute · GB

Funding

Department of Health NIHR-RP-011-048
6 · The paper itself

Abstract

Traumatic brain injury (TBI) leads to increased rates of dementia, including Alzheimer's disease. The mechanisms by which trauma can trigger neurodegeneration are increasingly understood. For example, diffuse axonal injury is implicated in disrupting microtubule function, providing the potential context for pathologies of tau and amyloid to develop. The neuropathology of post-traumatic dementias is increasingly well characterised, with recent work focusing on chronic traumatic encephalopathy (CTE). However, clinical diagnosis of post-traumatic dementia is problematic. It is often difficult to disentangle the direct effects of TBI from those produced by progressive neurodegeneration or other post-traumatic sequelae such as psychiatric impairment. CTE can only be confidently identified at postmortem and patients are often confused and anxious about the most likely cause of their post-traumatic problems. A new approach to the assessment of the long-term effects of TBI is needed. Accurate methods are available for the investigation of other neurodegenerative conditions. These should be systematically employed in TBI. MRI and positron emission tomography neuroimaging provide biomarkers of neurodegeneration which may be of particular use in the postinjury setting. Brain atrophy is a key measure of disease progression and can be used to accurately quantify neuronal loss. Fluid biomarkers such as neurofilament light can complement neuroimaging, representing sensitive potential methods to track neurodegenerative processes that develop after TBI. These biomarkers could characterise endophenotypes associated with distinct types of post-traumatic neurodegeneration. In addition, they might profitably be used in clinical trials of neuroprotective and disease-modifying treatments, improving trial design by providing precise and sensitive measures of neuronal loss.

Indexed as

Clinical Trials as TopicBiomarkersBrainBrain Injuries, TraumaticChronic Traumatic EncephalopathyDementiaDisease ProgressionHumansNerve DegenerationBiomarkersacquired brain injurycognitiondementiaimage analysistraumatic brain injury

Identifiers

PMID31542723
PMCPMC6860906
OpenAlexW2973476620

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.