Evidence map›Paper›PMID 31503421›Full record

ReviewCNS neuroscience & therapeutics2020

Exploring the bi-directional relationship between autophagy and Alzheimer's disease.

Huang Kuang, Cheng-Yong Tan, Hui-Zhen Tian, Li-Hua Liu, Mei-Wen Yang, Fen-Fang Hong, Shu-Long Yang

Open access · goldAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
6.5field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  7. Review
  8. Article
  9. Reinforcing Nrf2 Signaling: Help in the Alzheimer's Disease Context.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Review
  12. The role ofFrontiers in neuroscience · 2025
    Review
  13. Article
  14. Article
  15. 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

7 authors at 1 institution in 1 country.

Huang KuangDepartment of Physiology, College of Medicine, Nanchang University, Nanchang, China.ORCID 0000-0001-7739-291X
Cheng-Yong TanDepartment of Physiology, College of Medicine, Nanchang University, Nanchang, China.ORCID 0000-0002-4396-7479
Hui-Zhen TianDepartment of Physiology, College of Medicine, Nanchang University, Nanchang, China.ORCID 0000-0001-5928-6355
Li-Hua LiuDepartment of Physiology, College of Medicine, Nanchang University, Nanchang, China.ORCID 0000-0002-9456-9083
Mei-Wen YangDepartment of Nurse, Nanchang University Hospital, Nanchang, China.ORCID 0000-0002-8322-6181
Fen-Fang HongDepartment of Experimental Teaching Center, Nanchang University, Nanchang, China.ORCID 0000-0001-6440-1311
Shu-Long YangDepartment of Physiology, College of Medicine, Nanchang University, Nanchang, China.ORCID 0000-0002-1407-6255
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by β-amyloid (Aβ) deposition and Tau phosphorylation, in which its pathogenesis has not been cleared so far. The metabolism of Aβ and Tau is critically affected by the autophagy. Abnormal autophagy is thought to be involved in the pathogenesis of AD, regulating autophagy may become a new strategy for AD treatment. In the early stage of AD, the presence of Aβ and Tau can induce autophagy to promote their clearance by means of mTOR-dependent and independent manners. As AD progress, the autophagy goes aberrant. As a result, Aβ and Tau generate continually, which aggravates both autophagy dysfunction and AD. Besides, several related genes and proteins of AD can also adapt autophagy to make an effect on the AD development. There seems to be a bi-directional relationship between AD pathology and autophagy. At present, this article reviews this relationship from these aspects: (a) the signaling pathways of regulating autophagy; (b) the relationships between the autophagy and the processing of Aβ; (c) Aβ and Tau cause autophagy dysfunction; (d) normal autophagy promotes the clearance of Aβ and Tau; (e) the relationships between the autophagy and both genes and proteins related to AD: TFEB, miRNAs, Beclin-1, Presenilin, and Nrf2; and (f) the small molecules regulating autophagy on AD therapy. All of the above may help to further elucidate the pathogenesis of AD and provide a theoretical basis for clinical treatment of AD.

Indexed as

AutophagyAlzheimer DiseaseAmyloid beta-Protein PrecursorHumanstau ProteinsAmyloid beta-Protein PrecursorAPP protein, humanMAPT protein, humantau ProteinsAlzheimer's diseaseautophagygenes and proteinsTauβ-amyloid

Identifiers

PMID31503421
PMCPMC6978262
OpenAlexW2973034601

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.