Evidence map›Paper›PMID 10377346›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Mutant presenilin-1 induces apoptosis and downregulates Akt/PKB.

C C Weihl, G D Ghadge, S G Kennedy, N Hay, R J Miller, R P Roos

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 138 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Neuroprotective effects of ZL006 in AβNeural regeneration research · 2020
    Article
  6. Review
  7. Bax inhibitor 1 is a γ-secretase-independent presenilin-binding protein.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  8. Article
  9. CDK5 activator protein p25 preferentially binds and activates GSK3β.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Immunotherapy targeting pathological tau prevents cognitive decline in a new tangle mouse model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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

6 authors at 3 institutions in 2 countries.

C C WeihlCommittee on Neurobiology, University of Chicago, Chicago, Illinois 60637, USA.
G D Ghadge
S G Kennedy
N Hay
R J Miller
R P Roos
Committee on Climate Change · GBUniversity of Illinois Chicago · USUniversity of Chicago · US

Funding

VIRAL VECTORS IN THE STUDY OF ALZHEIMERS DISEASEF30MH011697 · NIMH · UNIVERSITY OF CHICAGO · PI WEIHL, CONRAD C · 1997 to 2000
$41k
NIMH NIH HHS F30 MH011697NIMH NIH HHS F30MH11697
6 · The paper itself

Abstract

Most early onset cases of familial Alzheimer's disease (AD) are caused by mutations in presenilin-1 (PS1) and presenilin-2 (PS2). These mutations lead to increased beta-amyloid formation and may induce apoptosis in some model systems. Using primary cultured hippocampal neurons (HNs) and rat pheochromocytoma (PC12) cells transiently transfected with replication-defective recombinant adenoviral vectors expressing wild-type or mutant PS1, we demonstrate that mutant PS1s induce apoptosis, downregulate the survival factor Akt/PKB, and affect several Akt/PKB downstream targets, including glycogen synthase kinase-3beta and beta-catenin. Expression of a constitutively active Akt/PKB rescues HNs from mutant PS1-induced neuronal cell death, suggesting a potential therapeutic target for AD. Downregulation of Akt/PKB may be a mechanism by which mutant PS1 induces apoptosis and may play a role in the pathogenesis of familial AD.

Indexed as

ApoptosisDown-RegulationMitogen-Activated Protein KinasesMutationReceptor, trkATrans-ActivatorsZebrafish ProteinsAdenoviridaeAlzheimer DiseaseAnimalsbeta CateninCalcium-Calmodulin-Dependent Protein KinasesCarrier ProteinsCells, CulturedCytoskeletal ProteinsEnzyme ActivationAkt1 protein, ratbeta CateninCalcium-Calmodulin-Dependent Protein KinasesCarrier ProteinsCtnnb1 protein, ratCytoskeletal ProteinsGlycogen Synthase Kinase 3Glycogen Synthase KinasesJNK Mitogen-Activated Protein KinasesMembrane ProteinsMitogen-Activated Protein KinasesNerve Growth FactorsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPresenilin-1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktReceptor, trkARibosomal Protein S6 KinasesTrans-ActivatorsWnt ProteinsZebrafish Proteins

Identifiers

PMID10377346
PMCPMC6782321
OpenAlexW1799837960

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.