Evidence map›Paper›PMID 37335158›Full record

ArticleJournal of food and drug analysis2023

Urolithin A exhibits a neuroprotective effect against Alzheimer's disease by inhibiting DYRK1A activity.

Huang-Ju Tu, Chih-Jou Su, Chao-Shiang Peng, Tony Eight Lin, Wei-Chun HuangFu, Kai-Cheng Hsu, Tsong-Long Hwang, Shiow-Lin Pan

Open access · hybridAbstract read
In one paragraph

Article in Journal of food and drug analysis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.4field-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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Urolithin A improves Alzheimer's disease cognition and restores mitophagy and lysosomal functions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  10. Review
  11. 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

8 authors at 2 institutions in 1 country.

Huang-Ju TuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Chih-Jou SuPh.D. Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Chao-Shiang PengPh.D. Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Tony Eight LinGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Wei-Chun HuangFuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Kai-Cheng HsuGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Tsong-Long HwangDepartment of Chemical Engineering, Ming Chi University of Technology, No.84 Gungjuan Rd., New Taipei City 243303, Taiwan.
Shiow-Lin PanGraduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, No.250, Wu-Xing Street, Xinyi Dist., Taipei 110, Taiwan.
Taipei Medical University · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease with more than 50 million people suffer from it. Unfortunately, none of the currently available drugs is able to improve cognitive impairment in AD patients. Urolithin A (UA) is a metabolite obtained from ellagic acid and ellagitannin through the intestinal flora, and it has antioxidant and anti-inflammatory properties. Previous reports found that UA had neuroprotective effects in an AD animal model, but the detailed mechanism still needs to be elucidated. In this study, we performed kinase-profiling to show that dual-specific tyrosine phosphorylation-regulated kinase 1A (DYRK1A) is the main target of UA. Studies showed that the level of DYRK1A in AD patients' brains was higher than that of healthy people, and it was closely related to the occurrence and progression of AD. Our results revealed that UA significantly reduced the activity of DYRK1A, which led to de-phosphorylation of tau and further stabilized microtubule polymerization. UA also provided neuroprotective effects by inhibiting the production of inflammatory cytokines caused by Aβ. We further showed that UA significantly improved memory impairment in an AD-like mouse model. In summary, our results indicate that UA is a DYRK1A inhibitor that may provide therapeutic advantages for AD patients.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesNeuroprotective AgentsAnimalsCoumarinsMice3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-oneCoumarinsNeuroprotective Agents

Identifiers

PMID37335158
PMCPMC10281726
OpenAlexW4380788632

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.