Evidence map›Paper›PMID 26316755›Full record

ArticleNeuropsychiatric disease and treatment2015

Autophagy dysfunction upregulates beta-amyloid peptides via enhancing the activity of γ-secretase complex.

Zhiyou Cai, Yingjun Zhou, Zhou Liu, Zunyu Ke, Bin Zhao

Open access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Treatment of Alzheimer's Disease: Beyond Symptomatic Therapies.International journal of molecular sciences · 2023
    Review
  6. Roles of Non-Coding RNA in Alzheimer's Disease Pathophysiology.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Autotaxin⁻Lysophosphatidic Acid Signaling in Alzheimer's Disease.International journal of molecular sciences · 2018
    Review
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Zhiyou CaiDepartment of Neurology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei Province, People's Republic of China.
Yingjun ZhouDepartment of Neurology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei Province, People's Republic of China.
Zhou LiuDepartment of Neurology, The Affiliated Hospital of Guangdong Medical College, Zhanjiang, Gangdong Province, People's Republic of China ; Institute of Neurology, Gangdong Medical College, Zhanjiang, Gangdong Province, People's Republic of China.
Zunyu KeDepartment of Neurology, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei Province, People's Republic of China.
Bin ZhaoDepartment of Neurology, The Affiliated Hospital of Guangdong Medical College, Zhanjiang, Gangdong Province, People's Republic of China ; Institute of Neurology, Gangdong Medical College, Zhanjiang, Gangdong Province, People's Republic of China.
Hubei University of Medicine · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies have shown that autophagy failure plays a critical role in the pathogenesis of Alzheimer's disease, including increased expression of beta-amyloid (Aβ) protein and the dysfunction of Aβ clearance. To further evaluate the role of autophagy in Alzheimer's disease, the present study was implemented to investigate the effects of autophagy on α-secretase, β-secretase, or γ-secretase, and observe the effects of autophagy on autophagic clearance markers. These results showed that both autophagy inhibitor and inducer enhanced the activity of α-, β-, and γ-secretases, and Aβ production. Autophagy inhibitor may more activate γ-secretase and promote Aβ production and accumulation than its inducer. Both autophagy inhibitor and inducer had no influence on Aβ clearance. Hence, autophagy inhibitor may activate γ-secretase and promote Aβ production and accumulation, but has no influence on Aβ clearance.

Indexed as

Alzheimer’s diseaseautophagybeta-amyloidsecretases

Identifiers

PMID26316755
PMCPMC4547656
OpenAlexW2145569054

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.