Evidence map›Paper›PMID 39269547›Full record

ReviewMolecular neurobiology2025

Role of Mitochondrial Dysfunctions in Neurodegenerative Disorders: Advances in Mitochondrial Biology.

Divya Sri Kathiresan, Rubadevi Balasubramani, Kamalesh Marudhachalam, Piyush Jaiswal, Nivedha Ramesh, Suruthi Gunna Sureshbabu, Vinayaga Moorthi Puthamohan, Murali Vijayan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

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  15. Puerarin Improves Cancer-Induced Bone Pain by Recovering Mitochondrial Dysfunction in the Spinal Cord.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  16. Review
  17. Genetic mutations in kinases: a comprehensive review on marketed inhibitors and unexplored targets in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  18. Article
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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

8 authors.

Divya Sri KathiresanDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Rubadevi BalasubramaniDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Kamalesh MarudhachalamDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Piyush JaiswalDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Nivedha RameshDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Suruthi Gunna SureshbabuDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India.
Vinayaga Moorthi PuthamohanDepartment of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, Nadu, Tamil, 641046, India. pvmhgmb@buc.edu.in.
Murali VijayanDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, 79430, USA. murali.vijayan@ttuhsc.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria, essential organelles responsible for cellular energy production, emerge as a key factor in the pathogenesis of neurodegenerative disorders. This review explores advancements in mitochondrial biology studies that highlight the pivotal connection between mitochondrial dysfunctions and neurological conditions such as Alzheimer's, Parkinson's, Huntington's, ischemic stroke, and vascular dementia. Mitochondrial DNA mutations, impaired dynamics, and disruptions in the ETC contribute to compromised energy production and heightened oxidative stress. These factors, in turn, lead to neuronal damage and cell death. Recent research has unveiled potential therapeutic strategies targeting mitochondrial dysfunction, including mitochondria targeted therapies and antioxidants. Furthermore, the identification of reliable biomarkers for assessing mitochondrial dysfunction opens new avenues for early diagnosis and monitoring of disease progression. By delving into these advancements, this review underscores the significance of understanding mitochondrial biology in unraveling the mechanisms underlying neurodegenerative disorders. It lays the groundwork for developing targeted treatments to combat these devastating neurological conditions.

Indexed as

MitochondriaNeurodegenerative DiseasesAnimalsDNA, MitochondrialHumansOxidative StressDNA, MitochondrialBiogenesisMitochondriaMtDNA dynamicsNeurodegenerationOxidative stressTherapeutics

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.