Evidence map›Paper›PMID 33379372›Full record

ReviewAntioxidants (Basel, Switzerland)2020

Potential Therapeutic Role of Phytochemicals to Mitigate Mitochondrial Dysfunctions in Alzheimer's Disease.

Md Ataur Rahman, Md Hasanur Rahman, Partha Biswas, Md Shahadat Hossain, Rokibul Islam, Md Abdul Hannan, Md Jamal Uddin, Hyewhon Rhim

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. Article
  8. Scientifica · 2026
    Article
  9. Mechanisms Underlying the Cognitive Benefits ofPlants (Basel, Switzerland) · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Research in pharmaceutical sciences · 2024
    Article
  19. Identification of antidiabetic inhibitors fromSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024
    Article
  20. 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 7 institutions in 2 countries.

Md Ataur RahmanCenter for Neuroscience, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.ORCID 0000-0001-6649-3694
Md Hasanur RahmanABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh.ORCID 0000-0001-9238-3149
Partha BiswasABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh.ORCID 0000-0002-9766-756X
Md Shahadat HossainABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh.ORCID 0000-0002-7940-2779
Rokibul IslamDepartment of Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia 7003, Bangladesh.
Md Abdul HannanDepartment of Anatomy, Dongguk University College of Medicine, Gyeongju 38066, Korea.ORCID 0000-0001-6640-4495
Md Jamal UddinABEx Bio-Research Center, East Azampur, Dhaka 1230, Bangladesh.ORCID 0000-0003-2911-3255
Hyewhon RhimCenter for Neuroscience, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.
Bio-Medical Science (South Korea) · KRDongguk University · KREwha Womans University · KRGopalganj Science and Technology University · BDHallym University · KRIslamic University · BDNoakhali Science and Technology University · BD

Funding

National Research Foundation of Korea 2016M3C7A1913845
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a decline in cognitive function and neuronal damage. Although the precise pathobiology of AD remains elusive, accumulating evidence suggests that mitochondrial dysfunction is one of the underlying causes of AD. Mutations in mitochondrial or nuclear DNA that encode mitochondrial components may cause mitochondrial dysfunction. In particular, the dysfunction of electron transport chain complexes, along with the interactions of mitochondrial pathological proteins are associated with mitochondrial dysfunction in AD. Mitochondrial dysfunction causes an imbalance in the production of reactive oxygen species, leading to oxidative stress (OS) and vice versa. Neuroinflammation is another potential contributory factor that induces mitochondrial dysfunction. Phytochemicals or other natural compounds have the potential to scavenge oxygen free radicals and enhance cellular antioxidant defense systems, thereby protecting against OS-mediated cellular damage. Phytochemicals can also modulate other cellular processes, including autophagy and mitochondrial biogenesis. Therefore, pharmacological intervention via neuroprotective phytochemicals can be a potential strategy to combat mitochondrial dysfunction as well as AD. This review focuses on the role of phytochemicals in mitigating mitochondrial dysfunction in the pathogenesis of AD.

Indexed as

Alzheimer’s diseaseautophagymitochondrial dysfunctionsphytochemicalsreactive oxygen species (ROS)

Identifiers

PMID33379372
PMCPMC7823298
OpenAlexW3109012073

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.