Evidence map›Paper›PMID 26957541›Full record

ArticleThe Journal of biological chemistry2016

Trehalose Alters Subcellular Trafficking and the Metabolism of the Alzheimer-associated Amyloid Precursor Protein.

Nguyen T Tien, Ilker Karaca, Irfan Y Tamboli, Jochen Walter

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Guideline
  2. Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
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  6. Article
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  12. Caveolae with serotonin and NMDA receptors as promising targets for the treatment of Alzheimer's disease.International journal of physiology, pathophysiology and pharmacology · 2024
    Review
  13. Trehalose improves the movement ability of AβTranslational neuroscience · 2024
    Article
  14. Article
  15. Review
  16. Mitophagy: An Emergence of New Player in Alzheimer's Disease.Frontiers in molecular neuroscience · 2022
    Review
  17. Article
  18. Article
  19. Fluorescent Protein-Based Autophagy Biosensors.Materials (Basel, Switzerland) · 2021
    Review
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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.

Nguyen T TienFrom the Department of Neurology, University of Bonn, 53127 Bonn, Germany.
Ilker KaracaFrom the Department of Neurology, University of Bonn, 53127 Bonn, Germany.
Irfan Y TamboliFrom the Department of Neurology, University of Bonn, 53127 Bonn, Germany.
Jochen WalterFrom the Department of Neurology, University of Bonn, 53127 Bonn, Germany jochen.walter@ukb.uni-bonn.de.ORCID http://orcid.org/0000-0002-4678-2912
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The disaccharide trehalose is commonly considered to stimulate autophagy. Cell treatment with trehalose could decrease cytosolic aggregates of potentially pathogenic proteins, including mutant huntingtin, α-synuclein, and phosphorylated tau that are associated with neurodegenerative diseases. Here, we demonstrate that trehalose also alters the metabolism of the Alzheimer disease-related amyloid precursor protein (APP). Cell treatment with trehalose decreased the degradation of full-length APP and its C-terminal fragments. Trehalose also reduced the secretion of the amyloid-β peptide. Biochemical and cell biological experiments revealed that trehalose alters the subcellular distribution and decreases the degradation of APP C-terminal fragments in endolysosomal compartments. Trehalose also led to strong accumulation of the autophagic marker proteins LC3-II and p62, and decreased the proteolytic activation of the lysosomal hydrolase cathepsin D. The combined data indicate that trehalose decreases the lysosomal metabolism of APP by altering its endocytic vesicular transport.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesAnimalsAutophagyCell LineHEK293 CellsHep G2 CellsHumansLysosomesMicePeptide FragmentsProtein TransportProteolysisSubcellular FractionsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesPeptide FragmentsTOR Serine-Threonine KinasesTrehaloseamyloid precursor protein (APP)amyloid-β (Aβ)autophagyendosomeintracellular traffickinglysosometrehalose

Identifiers

PMID26957541
PMCPMC4865903
OpenAlexW2293737369

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.