Evidence map›Paper›PMID 37436577›Full record

ArticleJournal of neurovirology2023

Cytomegalovirus infection induces Alzheimer's disease-associated alterations in tau.

Prapti H Mody, Kelsey N Marvin, DiAnna L Hynds, Laura K Hanson

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neurovirology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.5field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. The brain pathobiome in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. mFrontiers in cell and developmental biology · 2024
    Review
  19. 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

4 authors at 1 institution in 1 country.

Prapti H ModyDivision of Biology, Texas Woman's University, 304 Administration Drive, Denton, TX, 76204, USA.
Kelsey N MarvinDivision of Biology, Texas Woman's University, 304 Administration Drive, Denton, TX, 76204, USA.
DiAnna L HyndsDivision of Biology, Texas Woman's University, 304 Administration Drive, Denton, TX, 76204, USA.
Laura K HansonDivision of Biology, Texas Woman's University, 304 Administration Drive, Denton, TX, 76204, USA. lhanson@twu.edu.ORCID 0000-0002-1636-7187
Texas Woman's University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) manifests with loss of neurons correlated with intercellular deposition of amyloid (amyloid plaques) and intracellular neurofibrillary tangles of hyperphosphorylated tau. However, targeting AD hallmarks has not as yet led to development of an effective treatment despite numerous clinical trials. A better understanding of the early stages of neurodegeneration may lead to development of more effective treatments. One underexplored area is the clinical correlation between infection with herpesviruses and increased risk of AD. We hypothesized that similar to work performed with herpes simplex virus 1 (HSV1), infection with the cytomegalovirus (CMV) herpesvirus increases levels and phosphorylation of tau, similar to AD tauopathy. We used murine CMV (MCMV) to infect mouse fibroblasts and rat neuronal cells to test our hypothesis. MCMV infection increased steady-state levels of primarily high molecular weight forms of tau and altered the patterns of tau phosphorylation. Both changes required viral late gene products. Glycogen synthase kinase 3 beta (GSK3β) was upregulated in the HSVI model, but inhibition with lithium chloride suggested that this enzyme is unlikely to be involved in MCMV infection mediated tau phosphorylation. Thus, we confirm that MCMV, a beta herpes virus, like alpha herpes viruses (e.g., HSV1), can promote tau pathology. This suggests that CMV infection can be useful as another model system to study mechanisms leading to neurodegeneration. Since MCMV infects both mice and rats as permissive hosts, our findings from tissue culture can likely be applied to a variety of AD models to study development of abnormal tau pathology.

Indexed as

Alzheimer DiseaseCytomegalovirus InfectionsHerpesvirus 1, HumanAnimalsGlycogen Synthase Kinase 3 betaMiceNeuronsPhosphorylationRatstau ProteinsGlycogen Synthase Kinase 3 betatau ProteinsGlycogen synthase kinase 3 (GSK3)HerpesvirusLithium chloride (LiCl)Murine cytomegalovirus (MCMV)NeurodegenerationTau hyperphosphorylation

Identifiers

PMID37436577
OpenAlexW4383999230

What OpenQuestion holds

Textmetadata
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.