Evidence map›Paper›PMID 30403004›Full record

ReviewCNS neuroscience & therapeutics2019

Amyloid beta soluble forms and plasminogen activation system in Alzheimer's disease: Consequences on extracellular maturation of brain-derived neurotrophic factor and therapeutic implications.

Francesco Angelucci, Kateřina Čechová, Richard Průša, Jakub Hort

Open access · hybridAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.3field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. TheBrain plasticity (Amsterdam, Netherlands) · 2022
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. The functional and molecular roles of p75 neurotrophin receptor (p75Journal of central nervous system disease · 2024
    Review
  15. Serum Levels of Plasminogen Activator Inhibitor-1 in Patients with Parkinson's Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
    Article
  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

4 authors at 1 institution in 1 country.

Francesco AngelucciMemory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.ORCID 0000-0002-5956-5925
Kateřina ČechováMemory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
Richard PrůšaDepartment of Medical Chemistry and Clinical Biochemistry, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.ORCID 0000-0001-6408-7086
Jakub HortMemory Clinic, Department of Neurology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, Prague, Czech Republic.
Charles University · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Soluble oligomeric forms of amyloid beta (Aβ) play an important role in causing the cognitive deficits in Alzheimer's disease (AD) by targeting and disrupting synaptic pathways. Thus, the present research is directed toward identifying the neuronal pathways targeted by soluble forms and, accordingly, develops alternative therapeutic strategies. The neurotrophin brain-derived neurotrophic factor (BDNF) is synthesized as a precursor (pro-BDNF) which is cleaved extracellularly by plasmin to release the mature form. The conversion from pro-BDNF to BDNF is an important process that regulates neuronal activity and memory processes. Plasmin-dependent maturation of BDNF in the brain is regulated by plasminogen activator inhibitor-1 (PAI-1), the natural inhibitor of tissue-type plasminogen activator (tPA). Therefore, tPA/PAI-1 system represents an important regulator of extracellular BDNF/pro-BDNF ratio. In this review, we summarize the data on the components of the plasminogen activation system and on BDNF in AD. Moreover, we will hypothesize a possible pathogenic mechanism caused by soluble Aβ forms based on the effects on tPA/PAI-1 system and on the consequence of an altered conversion from pro-BDNF to the mature BDNF in the brain of AD patients. Translation into clinic may include a better characterization of the disease stage and future direction on therapeutic targets.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrain-Derived Neurotrophic FactorExtracellular SpaceHumansPlasminogenAmyloid beta-PeptidesBrain-Derived Neurotrophic FactorPlasminogenAlzheimer’s diseaseamyloid betabrain-derived neurotrophic factorplasminogen activator inhibitor-1tissue-type plasminogen activator

Identifiers

PMID30403004
PMCPMC6488905
OpenAlexW2899574118

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.