Evidence map›Paper›PMID 31642904›Full record

ReviewBiochemical Society transactions2019

Understanding PDE4's function in Alzheimer's disease; a target for novel therapeutic approaches.

Amy J Tibbo, Gonzalo S Tejeda, George S Baillie

Open access · hybridAbstract readReview
In one paragraph

Review in Biochemical Society transactions, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Protective effect of PDE4B subtype-specific inhibition in an App knock-in mouse model for Alzheimer's disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  12. PDE4D: A Multipurpose Pharmacological Target.International journal of molecular sciences · 2024
    Review
  13. Article
  14. cAMP/PKA signaling regulates TDP-43 aggregation and mislocalization.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

3 authors at 1 institution in 1 country.

Amy J TibboInstitute of Cardiovascular and Medical Science, College of Veterinary, Medical and Life Science, University of Glasgow, Glasgow, U.K.
Gonzalo S TejedaInstitute of Cardiovascular and Medical Science, College of Veterinary, Medical and Life Science, University of Glasgow, Glasgow, U.K.
George S BaillieInstitute of Cardiovascular and Medical Science, College of Veterinary, Medical and Life Science, University of Glasgow, Glasgow, U.K.
University of Glasgow · GB

Funding

British Heart Foundation BHF/TARGETPDE/PG/17/26/32881British Heart Foundation PG/17/26/32881Medical Research Council MC-PC-13063Medical Research Council MC_PC_13063Medical Research Council MC-PC-15039Medical Research Council MC_PC_15039
6 · The paper itself

Abstract

Phosphodiesterases (PDEs) have long been considered as targets for the treatment of Alzheimer's disease (AD) and a substantial body of evidence suggests that one sub-family from the super-family of PDEs, namely PDE4D, has particular significance in this context. This review discusses the role of PDE4 in the orchestration of cAMP response element binding signaling in AD and outlines the benefits of targeting PDE4D specifically. We examine the limited available literature that suggests PDE4 expression does not change in AD brains together with reports that show PDE4 inhibition as an effective treatment in this age-related neurodegenerative disease. Actually, aging induces changes in PDE4 expression/activity in an isoform and brain-region specific manner that proposes a similar complexity in AD brains. Therefore, a more detailed account of AD-related alterations in cellular/tissue location and the activation status of PDE4 is required before novel therapies can be developed to target cAMP signaling in this disease.

Indexed as

Alzheimer DiseaseAnimalsCREB-Binding ProteinCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4HumansSignal TransductionCREB-Binding ProteinCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 4Alzheimer's diseasecAMPcyclic nucleotide phosphodiesterases

Identifiers

PMID31642904
PMCPMC6824677
OpenAlexW2981371763

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.