Evidence map›Paper›PMID 26342176›Full record

ArticleJournal of neurochemistry2015

Soluble amyloid precursor protein alpha inhibits tau phosphorylation through modulation of GSK3β signaling pathway.

Juan Deng, Ahsan Habib, Demian F Obregon, Steven W Barger, Brian Giunta, Yan-Jiang Wang, Huayan Hou, Darrell Sawmiller, Jun Tan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Effects of Gelatin Hydrolysate from Bigeye Snapper (International journal of molecular sciences · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Alzheimer's Disease and Cancer: Common Targets.Mini reviews in medicinal chemistry · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  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

9 authors at 3 institutions in 2 countries.

Juan DengRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
Ahsan HabibRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
Demian F ObregonRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
Steven W BargerDepartment of Geriatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Brian GiuntaNeuroimmunology Laboratory, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, University of South Florida, Tampa, Florida, USA.
Yan-Jiang WangDepartment of Neurology and Center for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China.
Huayan HouRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
Darrell SawmillerRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
Jun TanRashid Laboratory for Developmental Neurobiology, Department of Psychiatry & Behavioral Neurosciences, Morsani College of Medicine, Silver Child Development Center, University of South Florida, Tampa, Florida, USA.
University of South Florida · USArmy Medical University · CNUniversity of Arkansas for Medical Sciences · US

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
Implication of HUCBC: a novel therapeutic strategy for Alzheimer's diseaseR01AG032432 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2009 to 2013
$1.4M
Flavonoid-diosmin modulation of Abeta and tau pathologies through GSK-3 signalingR01AT007411 · NCCIH · UNIVERSITY OF SOUTH FLORIDA · PI TAN, JUN · 2014 to 2015
$663k
Secreted Alzheimer amyloid precursor protein (sAPP) antagonizes Reelin receptorsR21AG033215 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI BARGER, STEVEN W · 2010 to 2011
$332k
NCCIH NIH HHS R01 AT007411NCCIH NIH HHS R01AT007411NIA NIH HHS P01 AG012411NIA NIH HHS P01AG012411NIA NIH HHS R01 AG032432NIA NIH HHS R01AG032432NIA NIH HHS R21 AG033215NIA NIH HHS R21AG033215
6 · The paper itself

Abstract

We recently found that sAPPα decreases amyloid-beta generation by directly associating with β-site amyloid precursor protein (APP)-converting enzyme 1 (BACE1), thereby modulating APP processing. Because inhibition of BACE1 decreases glycogen synthase kinase 3 beta (GSK3β)-mediated Alzheimer's disease (AD)-like tau phosphorylation in AD patient-derived neurons, we determined whether sAPPα also reduces GSK3β-mediated tau phosphorylation. We initially found increased levels of inhibitory phosphorylation of GSK3β (Ser9) in primary neurons from sAPPα over-expressing mice. Further, recombinant human sAPPα evoked the same phenomenon in SH-SY5Y cells. Further, in SH-SY5Y cells over-expressing BACE1, and HeLa cells over-expressing human tau, sAPPα reduced GSK3β activity and tau phosphorylation. Importantly, the reductions in GSK3β activity and tau phosphorylation elicited by sAPPα were prevented by BACE1 but not γ-secretase inhibition. In accord, AD mice over-expressing human sAPPα had less GSK3β activity and tau phosphorylation compared with controls. These results implicate a direct relationship between APP β-processing and GSK3β-mediated tau phosphorylation and further define the central role of sAPPα in APP autoregulation and AD pathogenesis.

Indexed as

Amyloid beta-Protein PrecursorAnimalsCell Line, TumorCells, CulturedDose-Response Relationship, DrugGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMiceMice, Inbred C57BLPhosphorylationSignal Transductiontau ProteinsAmyloid beta-Protein PrecursorGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mousetau ProteinsAlzheimer's diseaseBACE1GSK3βsAPPαtau

Identifiers

PMID26342176
PMCPMC4624213
OpenAlexW1903012165

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.