Evidence map›Paper›PMID 31488728›Full record

ArticleAging2019

Enhancing the retrograde axonal transport by curcumin promotes autophagic flux in N2a/APP695swe cells.

Jie Liang, Fanlin Zhou, Xiaomin Xiong, Xiong Zhang, Shijie Li, Xiaoju Li, Minna Gao, Yu Li

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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  13. Article
  14. Autophagy in Neurodegenerative Diseases: A Hunter for Aggregates.International journal of molecular sciences · 2020
    Review
  15. Natural Compounds and Autophagy: Allies Against Neurodegeneration.Frontiers in cell and developmental biology · 2020
    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

8 authors at 1 institution in 1 country.

Jie LiangDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Fanlin ZhouDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Xiaomin XiongDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Xiong ZhangInstitute of Neuroscience, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Shijie LiDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Xiaoju LiDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Minna GaoDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Yu LiDepartment of Pathology, School of Basic Medicine, Chongqing Medical University, Chongqing 400016, China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accumulation of autophagosomes and dysfunction at the axonal terminal of neurons play crucial roles in the genesis and development of Alzheimer's disease (AD). Abnormalities in neuron axonal transport-related proteins prevent autophagosome maturation in AD. Curcumin, a polyphenol plant compound, has been shown to exert neuroprotective effects by increasing autophagy in AD, but the underlying mechanism of its effect on autophagy axon transport remains elusive. This study investigated the effects of curcumin on autophagosome formation and axonal transport in N2a/APP695swe cells (AD cell model) as well as the mechanism underlying those effects. Curcumin treatment significantly increased the expression of Beclin1, Atg5, and Atg16L1, induced the formation of autophagosomes, and promoted autophagosome-lysosome fusion in N2a/APP695swe cells. At the same time, curcumin promoted the expression of dynein, dynactin, and BICD2 as well as their binding to form the retrograde axonal transport molecular motor complex. Moreover, curcumin also increased the expression of the scaffolding proteins Rab7- interacting lysosomal protein (RILP) and huntingtin in N2a/APP695swe cells. Taken together, our findings indicate that curcumin increases autophagic flux by promoting interactions among autophagic axonal transport-related proteins and inducing lysosome-autophagosome fusion. This study provides evidence suggesting the potential use of curcumin as a novel treatment for AD.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalAutophagosomesAutophagyAxonal TransportCell Line, TumorCurcuminDynactin ComplexGene ExpressionMiceMicrotubule-Associated ProteinsAnti-Inflammatory Agents, Non-SteroidalBicd2 protein, mouseCurcuminDynactin ComplexMicrotubule-Associated ProteinsAlzheimer’s diseaseautophagyaxonal transportcurcumindynein

Identifiers

PMID31488728
PMCPMC6756876
OpenAlexW2971800897

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.