Evidence map›Paper›PMID 31561367›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Long-Term Effects of Traumatic Brain Injury in a Mouse Model of Alzheimer's Disease.

Marlena Zyśk, Fredrik Clausen, Ximena Aguilar, Dag Sehlin, Stina Syvänen, Anna Erlandsson

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
  2. Article
  3. Limitations of Current Therapies and Barriers in Alzheimer's Disease.Archives of internal medicine research · 2026
    Article
  4. History of Traumatic Brain Injury with Loss of Consciousness and APOEbioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Genetic predisposition to Alzheimer's disease alters inflammasome activity after traumatic brain injury.Translational research : the journal of laboratory and clinical medicine · 2023
    Article
  12. Review
  13. Inflammasome activation in traumatic brain injury and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors.

Marlena ZyśkDepartment of Public Health and Caring Sciences, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.
Fredrik ClausenDepartment of Neuroscience, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.
Ximena AguilarDepartment of Public Health and Caring Sciences, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.
Dag SehlinDepartment of Public Health and Caring Sciences, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.
Stina SyvänenDepartment of Public Health and Caring Sciences, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.
Anna ErlandssonDepartment of Public Health and Caring Sciences, Uppsala University, Rudbeck Laboratory, Uppsala, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the leading cause of dementia worldwide, affecting over 10% of the elderly population. Epidemiological evidence indicates that traumatic brain injury (TBI) is an important risk factor for developing AD later in life. However, which injury-induced processes that contribute to the disease onset remains unclear. The aim with the present study was to identify cellular processes that could link TBI to AD development, by investigating the chronic impact of two different injury models, controlled cortical impact (CCI) and midline fluid percussion injury (mFPI). The trauma was induced in 3-month-old tg-ArcSwe mice, carrying the Arctic mutation along with the Swedish mutation, and the influence of TBI on AD progression was analyzed at 12- and 24-weeks post-injury. The long-term effect of the TBI on memory deficiency, amyloid-β (Aβ) pathology, neurodegeneration and inflammation was investigated by Morris water maze, PET imaging, immunohistochemistry, and biochemical analyses. Morris water maze analysis demonstrated that mice subjected to CCI or mFPI performed significantly worse than uninjured tg-ArcSwe mice, especially at the later time point. Moreover, the injured mice showed a late upregulation of reactive gliosis, which concurred with a more pronounced Aβ pathology, compared to uninjured AD mice. Our results suggest that the delayed glial activation following TBI may be an important link between the two diseases. However, further studies in both experimental models and human TBI patients will be required to fully elucidate the reasons why TBI increases the risk of neurodegeneration.

Indexed as

Disease Models, AnimalAlzheimer DiseaseAnimalsBrain Injuries, TraumaticFemaleMaleMemory DisordersMiceMice, Inbred C57BLMice, TransgenicPositron-Emission TomographyTime FactorsAlzheimer’s diseaseamyloid-βinflammationMorris water mazeneurodegeneration astrocytesPETtraumatic brain injury

Identifiers

PMID31561367
PMCPMC6839469

What OpenQuestion holds

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LicenceCC BY-NC
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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 OpenQuestion graph.