Evidence map›Paper›PMID 20351282›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

PI3 kinase signaling is involved in Abeta-induced memory loss in Drosophila.

Hsueh-Cheng Chiang, Lei Wang, Zuolei Xie, Alice Yau, Yi Zhong

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
4.1field-weighted citation impact, top 6% 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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Article
  8. Correlation between plasma epidermal growth factor and follow-up cognitive decline in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
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  15. The role of PI3K signaling pathway in Alzheimer's disease.Frontiers in aging neuroscience · 2024
    Review
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  17. Article
  18. Review
  19. Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

Hsueh-Cheng ChiangCold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Lei Wang
Zuolei Xie
Alice Yau
Yi Zhong
Cold Spring Harbor Laboratory · USStony Brook University · USTsinghua University · CN

Funding

RAS/RAF PATHWAY IN NEUROTRANSMISSION IN DROSOPHILAR01NS034779 · NINDS · COLD SPRING HARBOR LABORATORY · PI ZHONG, YI · 1996 to 2003
$1.2M
NINDS NIH HHS 2R01 NS34779-06NINDS NIH HHS R01 NS034779
6 · The paper itself

Abstract

Multiple intracellular signals are altered in Alzheimer's disease brain tissues, including the PI3K/Akt pathway. However, the pathological relevance of such alterations is poorly understood. In vitro studies yield results that seem to be consistent with the conventional perception in which an up-regulation of the cell survival pathway, PI3K pathway, is protective in Alzheimer's disease pathogenesis. The current in vivo genetic approach, however, reveals that inhibition of the PI3K pathway leads to rescuing of the beta-amyloid peptide (Abeta)-induced memory loss in the Drosophila brain. We began our inquiry into the molecular basis of this memory loss by studying Abeta42-induced enhancement of long-term depression. We found that long-term depression is restored to a normal level through inhibition of PI3K activity. Abeta42-induced PI3K hyperactivity is directly confirmed by immunostaining of the PI3K phosphorylation targets, phospholipids. Such observations lead to the following demonstration that Abeta42-induced memory loss can be rescued through genetic silencing or pharmacological inhibition of PI3K functions. Our data suggest that Abeta42 stimulates PI3K, which in turn causes memory loss in association with an increase in accumulation of Abeta42 aggregates.

Indexed as

Amyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedDisease Models, AnimalDrosophila melanogasterElectrophysiologyLearningLipidsMemoryMemory DisordersModels, BiologicalModels, GeneticNeurodegenerative DiseasesPhosphatidylinositol 3-KinasesPhosphorylationSmellAmyloid beta-PeptidesLipidsPhosphatidylinositol 3-Kinases

Identifiers

PMID20351282
PMCPMC2872421
OpenAlexW2029377385

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.