Evidence map›Paper›PMID 20555131›Full record

ArticleJournal of Alzheimer's disease : JAD2010

Reductions in amyloid-beta-derived neuroinflammation, with minocycline, restore cognition but do not significantly affect tau hyperphosphorylation.

Anna Parachikova, Vitaly Vasilevko, David H Cribbs, Frank M LaFerla, Kim N Green

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Drug repositioning for Alzheimer's disease.Nature reviews. Drug discovery · 2012
    Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. The brain pathobiome in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Repurposing Licensed Drugs for Use Against Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  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

5 authors at 1 institution in 1 country.

Anna ParachikovaInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA 92697-4545, USA.
Vitaly Vasilevko
David H Cribbs
Frank M LaFerla
Kim N Green
University of California, Irvine · US

Funding

UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI COTMAN, CARL WAYNE · 1985 to 2018
$24.8M
Multiple Approaches to Abeta Vaccination in Animal ModelsR01AG020241 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI AGADJANYAN, MICHAEL G, CRIBBS, DAVID HASTINGS · 2001 to 2016
$5.6M
Multiple Approaches to Abeta Vaccination in Animal ModelsRF1AG020241 · NIA · INSTITUTE FOR MOLECULAR MEDICINE · PI AGADJANYAN, MICHAEL G, CRIBBS, DAVID HASTINGS · 2018 to 2018
$3.3M
Gene Interactions in a Model of Alzheimer's DiseaseR01AG021982 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2003 to 2012
$3.3M
NIA NIH HHS AG000538NIA NIH HHS AG020241NIA NIH HHS AG0212982NIA NIH HHS P01 AG000538NIA NIH HHS P50 AG016573NIA NIH HHS P50 AG16573NIA NIH HHS R01 AG020241NIA NIH HHS R01 AG021982NIA NIH HHS RF1 AG020241
6 · The paper itself

Abstract

Cognitive decline in Alzheimer's disease (AD) occurs as a result of the buildup of pathological proteins and downstream events including an elevated and altered inflammatory response. Inflammation has previously been linked to increased abnormal phosphorylation of tau protein. To determine if endogenous amyloid-beta (Abeta)-induced neuroinflammation drives tau phosphorylation in vivo, we treated 8-month-old 3xTg-AD with minocycline, an anti-inflammatory agent, to assess how it influenced cognitive decline and development of pathology. 4 months of treatment restored cognition to non-transgenic performance. Inflammatory profiling revealed a marked decrease in GFAP, TNFalpha, and IL6 and an increase in the CXCL1 chemokines KC and MIP1a. Minocycline also reduced levels of insoluble Abeta and soluble fibrils. Despite reducing levels of the tau kinase cdk5 coactivator p25, minocycline did not have wide effects on tau pathology with only one phospho-epitope showing reduction with treatment (S212/S214). The sum of these findings shows that reduction of the inflammatory events in an AD mouse model prevents cognitive deficits associated with pathology, but that endogenous Abeta-derived neuroinflammation does not contribute significantly to the development of tau pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnti-Bacterial AgentsCognitionDisease Models, AnimalEncephalitisMaze LearningMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicMinocyclinePhosphorylationRecognition, PsychologyTauopathiesAmyloid beta-PeptidesAnti-Bacterial AgentsMinocyclinetau Proteins

Identifiers

PMID20555131
PMCPMC4085054
OpenAlexW1566600743

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.