Evidence map›Paper›PMID 34364650›Full record

ReviewBiological psychiatry2022

Traumatic Brain Injury and Risk of Neurodegenerative Disorder.

Benjamin L Brett, Raquel C Gardner, Jonathan Godbout, Kristen Dams-O'Connor, C Dirk Keene

Open access · greenAbstract readReview
In one paragraph

Review in Biological psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 4 pooled it
33.1field-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

252 citing papers in PubMed, 4 syntheses or guidelines pooled it, 381 citations in OpenAlex.

  1. Pooled it
  2. Long-term life expectancy in severe traumatic brain injury: a systematic review.European journal of physical and rehabilitation medicine · 2024
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Beyond Histamine Blockade: Clemastine Fumarate as a Promoter of Myelin Regeneration, Inflammatory Regulation, and Neuroimmune Modulation in CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Review
  7. Traumatic brain injury induces cell-type-specific remodelling of the proteostasis network.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Article
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192 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

5 authors at 5 institutions in 1 country.

Benjamin L BrettDepartment of Neurosurgery, Medical College of Wisconsin, Milwaukee, Wisconsin. Electronic address: bbrett@mcw.edu.
Raquel C GardnerDepartment of Neurology, Memory and Aging Center, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, California; San Francisco Veterans Affairs Medical Center, San Francisco, California.
Jonathan GodboutDepartment of Neuroscience, Chronic Brain Injury Program, The Ohio State Wexner Medical Center, Columbus, Ohio.
Kristen Dams-O'ConnorDepartment of Rehabilitation and Human Performance, Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York.
C Dirk KeeneDepartment of Laboratory Medicine and Pathology, University of Washington School of Medicine, Seattle, Washington.
Icahn School of Medicine at Mount Sinai · USMedical College of Wisconsin · USSan Francisco VA Medical Center · USThe Ohio State University Wexner Medical Center · USUniversity of Washington · US

Funding

University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI Amanda D. Boyd · 2020 to 2026
$29.0M
Traumatic Brain Injury and Repetitive Head Impacts: Contributions to AD/ADRD and CTE Neuropathology and Resulting Clinical SyndromesU54NS115266 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STEIN, THOR · 2019 to 2023
$10.3M
The Late Effects of TBI (LETBI) Study: Injury Patterns and Biological Markers of Post-Traumatic NeurodegenerationRF1NS115268 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Kristen Dams-O'Connor · 2019 to 2026
$10.3M
Data Coordinating CoreU54NS115322 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 2019 to 2023
$9.2M
Leveraging Existing Aging Research Networks to investigate TBI and AD/ADRD risk (LEARN TBI & AD)R01AG061028 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAMS-O'CONNOR, KRISTEN, MEZ, JESSE BENJAMIN · 2019 to 2023
$5.9M
Chronic and Evolving Inflammation after Traumatic Brain Injury: Microglial Priming and Neuropsychiatric ComplicationsR01NS118037 · NINDS · OHIO STATE UNIVERSITY · PI GODBOUT, JONATHAN P · 2021 to 2025
$2.2M
ACL HHS 90DPTB0009NIA NIH HHS P30 AG066509NIA NIH HHS R01 AG061028NINDS NIH HHS L30 NS113158NINDS NIH HHS R01 NS118037NINDS NIH HHS RF1 NS115268NINDS NIH HHS U54 NS115266NINDS NIH HHS U54 NS115322
6 · The paper itself

Abstract

Traumatic brain injury (TBI), particularly of greater severity (i.e., moderate to severe), has been identified as a risk factor for all-cause dementia and Parkinson's disease, with risk for specific dementia subtypes being more variable. Among the limited studies involving neuropathological (postmortem) confirmation, the association between TBI and risk for neurodegenerative disease increases in complexity, with polypathology often reported on examination. The heterogeneous clinical and neuropathological outcomes associated with TBI are likely reflective of the multifaceted postinjury acute and chronic processes that may contribute to neurodegeneration. Acutely in TBI, axonal injury and disrupted transport influences molecular mechanisms fundamental to the formation of pathological proteins, such as amyloid-β peptide and hyperphosphorylated tau. These protein deposits may develop into amyloid-β plaques, hyperphosphorylated tau-positive neurofibrillary tangles, and dystrophic neurites. These and other characteristic neurodegenerative disease pathologies may then spread across brain regions. The acute immune and neuroinflammatory response involves alteration of microglia, astrocytes, oligodendrocytes, and endothelial cells; release of downstream pro- and anti-inflammatory cytokines and chemokines; and recruitment of peripheral immune cells. Although thought to be neuroprotective and reparative initially, prolongation of these processes may promote neurodegeneration. We review the evidence for TBI as a risk factor for neurodegenerative disorders, including Alzheimer's dementia and Parkinson's disease, in clinical and neuropathological studies. Further, we describe the dynamic interactions between acute response to injury and chronic processes that may be involved in TBI-related pathogenesis and progression of neurodegeneration.

Indexed as

Alzheimer DiseaseBrain Injuries, TraumaticNeurodegenerative DiseasesParkinson DiseaseBrainEndothelial CellsHumansDementiaNeurodegenerationNeuroinflammationNeuropathologyTraumatic brain injury

Identifiers

PMID34364650
PMCPMC8636548
OpenAlexW3170885926

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.