Evidence map›Paper›PMID 29396300›Full record

ReviewEBioMedicine2018

Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link.

Jaime Ramos-Cejudo, Thomas Wisniewski, Charles Marmar, Henrik Zetterberg, Kaj Blennow, Mony J de Leon, Silvia Fossati

2 registry-linked trialsOpen access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 226 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 5 pooled it
20.2field-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.

NCT04744051 phase1unknown statusnot on this mapstarted 2021, after this paper: background citation

ATCell™ Expanded Autologous, Adipose-Derived Mesenchymal Stem Cells Deployed Via Intravenous Infusion for the Treatment of Post Concussion Syndrome (PCS) in Retired Military and Athletes

TypeinterventionalSponsorAmerican CryoStem CorporationRan2021 to 2024Enrolled20ConditionsPost-Concussion SyndromeArms50 Adipose Derived Stem Cell Infusion, 150 Adipose Derived Stem Cell Infusion, 300 Adipose Derived Stem Cell Infusion, Placebo Infusion
NCT06480838 recruitingnot on this mapstarted 2023, after this paper: background citation

Cerebral Autoregulation, Brain Perfusion, and Neurocognitive Outcomes After Traumatic Brain Injury

TypeobservationalSponsorUniversity of Texas Southwestern Medical CenterRan2023 to 2029Enrolled130ConditionsTraumatic Brain Injury With Loss of Consciousness, Brain Injury Traumatic Severe, Brain Injury Traumatic Moderate, TBI (Traumatic Brain Injury)
3 · Its place in the literature

Who cites it

226 citing papers in PubMed, 5 syntheses or guidelines pooled it, 376 citations in OpenAlex.

  1. Pooled it
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  6. Trial
  7. Article
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  9. Review
  10. The landscape of dementia in India: Prevalence, risk factors, and opportunities ahead.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  11. Article
  12. Traumatic brain injury and risk of early-onset dementia: A population-based cohort study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  13. Article
  14. Article
  15. Vascular contribution to cognitive impairment and dementia (VCID): proceedings of 2025 workshop of the Jackson Laboratory.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  16. Review
  17. Article
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166 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 3 countries.

Jaime Ramos-CejudoNew York University, School of Medicine, Department of Psychiatry, New York, NY, USA.
Thomas WisniewskiNew York University, School of Medicine, Department of Psychiatry, New York, NY, USA; New York University, School of Medicine, Center for Cognitive Neurology, Department of Neurology, New York, NY, USA; New York University, School of Medicine, Department of Pathology, New York, NY, USA.
Charles MarmarNew York University, School of Medicine, Department of Psychiatry, New York, NY, USA.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, United Kingdom.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Mony J de LeonNew York University, School of Medicine, Department of Psychiatry, New York, NY, USA.
Silvia FossatiNew York University, School of Medicine, Department of Psychiatry, New York, NY, USA; New York University, School of Medicine, Center for Cognitive Neurology, Department of Neurology, New York, NY, USA. Electronic address: Silvia.Fossati@nyumc.org.
New York University · USSahlgrenska University Hospital · SE

Funding

PSYCHOSOCIAL COREP30AG008051 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SHAO, YONGZHAO · 1990 to 2019
$36.1M
PREDICTORS OF COGNITIVE DECLINE IN NORMAL AGINGR01AG012101 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J., RUSINEK, HENRY · 1993 to 2015
$6.7M
CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ADR01AG013616 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J. · 1995 to 2013
$6.2M
Biomarkers in Early Alzheimer's Disease (AD).R01AG022374 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DE LEON, MONY J., RUSINEK, HENRY · 2004 to 2015
$5.2M
Therapeutic Targeting of Abnormal Conformation in Neurodegenerative DiseaseR01NS073502 · NINDS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2010 to 2019
$3.7M
NIA NIH HHS P30 AG008051NIA NIH HHS R01 AG012101NIA NIH HHS R01 AG013616NIA NIH HHS R01 AG022374NINDS NIH HHS R01 NS073502
6 · The paper itself

Abstract

Traumatic brain injury (TBI) and Alzheimer's disease (AD) are devastating neurological disorders, whose complex relationship is not completely understood. Cerebrovascular pathology, a key element in both conditions, could represent a mechanistic link between Aβ/tau deposition after TBI and the development of post concussive syndrome, dementia and chronic traumatic encephalopathy (CTE). In addition to debilitating acute effects, TBI-induced neurovascular injuries accelerate amyloid β (Aβ) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/Aβ-induced blood brain barrier damage, giving rise to a deleterious feed-forward loop. We postulate that TBI can initiate cerebrovascular pathology, which is causally involved in the development of multiple forms of neurodegeneration including AD-like dementias. In this review, we will explore how novel biomarkers, animal and human studies with a focus on cerebrovascular dysfunction are contributing to the understanding of the consequences of TBI on the development of AD-like pathology.

Indexed as

Cerebrovascular CirculationAlzheimer DiseaseAnimalsBlood-Brain BarrierBrain Injuries, TraumaticEndothelial CellsHumansMitochondriaAlzheimer's diseaseAβBiomarkersCerebrovascular pathologyTauTraumatic brain injury

Identifiers

PMID29396300
PMCPMC5835563
OpenAlexW2790028019

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.