Evidence map›Paper›PMID 30499006›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2019

CNS-Wide over Expression of Fractalkine Improves Cognitive Functioning in a Tauopathy Model.

Dylan J Finneran, Dave Morgan, Marcia N Gordon, Kevin R Nash

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. The innate immune response in tauopathies.European journal of immunology · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Microglia Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2021
    Review
  19. Physical Exercise-Induced Myokines in Neurodegenerative Diseases.International journal of molecular sciences · 2021
    Review
  20. Review
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

4 authors at 2 institutions in 1 country.

Dylan J FinneranDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Byrd Alzheimer's Institute, 4001 E Fletcher Ave, Tampa, FL, 33617, USA.
Dave MorganTranslational Science and Molecular Medicine, Michigan State University, GRRC, 400 Monroe Ave. NW, Grand Rapids, MI, 49503, USA.
Marcia N GordonTranslational Science and Molecular Medicine, Michigan State University, GRRC, 400 Monroe Ave. NW, Grand Rapids, MI, 49503, USA.
Kevin R NashDepartment of Molecular Pharmacology & Physiology, Morsani College of Medicine, University of South Florida, Byrd Alzheimer's Institute, 4001 E Fletcher Ave, Tampa, FL, 33617, USA. knash@health.usf.edu.
Michigan State University · USUniversity of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence increasingly implicates regulation of neuroinflammation as a potential therapeutic target in Alzheimer's disease and other neurodegenerative disorders. Fractalkine (FKN) is a unique chemokine that is expressed and secreted by neurons and reduces expression of pro-inflammatory genes. To further demonstrate the utility of agents that increase FKN signaling throughout the central nervous system as possible therapies for AD, we assessed the impact of soluble FKN (sFKN) over expression on cognition in tau depositing rTg450 mice after the onset of cognitive deficits. Using adeno-associated virus serotype 4, we infected cells lining the ventricular system with soluble FKN to increase FKN signaling over a larger fraction of the brain than achieved with intraparenchymal injections. We found that soluble FKN over expression by cells lining the ventricles significantly improved cognitive performance on the novel mouse recognition and radial arm water maze tasks. These benefits were achieved without detectable reductions in tau hyperphosphorylation, hippocampal atrophy, or microglial CD45 expression. Utilizing qPCR, we report a significant increase in Vegfa expression, indicating an increase in trophic support and possible neovascularization in AAV-sFKN-injected mice. To our knowledge, this is the first demonstration that FKN over expression can rescue cognitive function in a tau depositing mouse line. Graphical Abstract Regulating neuroinflammation is an attractive therapeutic target for Alzheimer's disease. Microglial activation can not only drive pathology but also accelerate cognitive decline. The chemokine fractalkine regulates the microglial phenotype, increasing trophic support of neurons, and significantly improving cognitive functioning in the rTg4510 mouse model of tauopathy.

Indexed as

CognitionAnimalsCentral Nervous SystemCerebral VentriclesChemokine CX3CL1Cognition DisordersHippocampusLeukocyte Common AntigensMiceNeovascularization, PhysiologicSignal TransductionTauopathiesVascular Endothelial Growth Factor AChemokine CX3CL1Cx3cl1 protein, mouseLeukocyte Common AntigensPtprc protein, mouseVascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseAlzheimer’s diseaseCX3CL1FractalkineMicrogliaTauopathy

Identifiers

PMID30499006
PMCPMC6525127
OpenAlexW2903515625

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.