Evidence map›Paper›PMID 22849382›Full record

ReviewJournal of neuroinflammation2012

The immunology of traumatic brain injury: a prime target for Alzheimer's disease prevention.

Brian Giunta, Demian Obregon, Renuka Velisetty, Paul R Sanberg, Cesar V Borlongan, Jun Tan

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

Review in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03089749 (Characterization of Human Autoantibody Titers After Central Nervous System Insult), which is not on this map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
6.6field-weighted citation impact, top 3% 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.

NCT03089749 terminatednot on this mapstarted 2015, after this paper: background citation

Characterization of Human Autoantibody Titers After Central Nervous System Insult

TypeobservationalSponsorUniversity of UtahRan2015 to 2019Enrolled63ConditionsBrain Injuries, Traumatic, Spinal Cord Trauma, Intracranial Neoplasm
3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.International journal of molecular sciences · 2024
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review

13 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

6 authors at 2 institutions in 1 country.

Brian GiuntaJames A. Haley Veterans' Administration Hospital, 13000 Bruce B. Downs Blvd., Tampa, FL 33612, USA. bgiunta@health.usf.edu
Demian Obregon
Renuka Velisetty
Paul R Sanberg
Cesar V Borlongan
Jun Tan
University of South Florida · USJames A. Haley Veterans' Hospital · US

Funding

The impact of HAART on HIV-1 Tat induced brain agingR01MH098737 · NIMH · UNIVERSITY OF SOUTH FLORIDA · PI GIUNTA, BRIAN · 2012 to 2015
$1.3M
NIMH NIH HHS R01 MH098737
6 · The paper itself

Abstract

A global health problem, traumatic brain injury (TBI) is especially prevalent in the current era of ongoing world military conflicts. Its pathological hallmark is one or more primary injury foci, followed by a spread to initially normal brain areas via cascades of inflammatory cytokines and chemokines resulting in an amplification of the original tissue injury by microglia and other central nervous system immune cells. In some cases this may predispose individuals to later development of Alzheimer's disease (AD). The inflammatory-based progression of TBI has been shown to be active in humans for up to 17 years post TBI. Unfortunately, all neuroprotective drug trials have failed, and specific treatments remain less than efficacious. These poor results might be explained by too much of a scientific focus on neurons without addressing the functions of microglia in the brain, which are at the center of proinflammatory cytokine generation. To address this issue, we provide a survey of the TBI-related brain immunological mechanisms that may promote progression to AD. We discuss these immune and microglia-based inflammatory mechanisms involved in the progression of post-trauma brain damage to AD. Flavonoid-based strategies to oppose the antigen-presenting cell-like inflammatory phenotype of microglia will also be reviewed. The goal is to provide a rationale for investigations of inflammatory response following TBI which may represent a pathological link to AD. In the end, a better understanding of neuroinflammation could open therapeutic avenues for abrogation of secondary cell death and behavioral symptoms that may mediate the progression of TBI to later AD.

Indexed as

Disease ProgressionAlzheimer DiseaseAnimalsBrainBrain InjuriesHumansInflammation MediatorsInflammation Mediators

Identifiers

PMID22849382
PMCPMC3458981
OpenAlexW2097143517

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.