Evidence map›Paper›PMID 40813952›Full record

ReviewTissue barriers2026

Mitochondrial dysfunction and oxidative stress in Parkinson's disease: mechanisms, biomarkers, and therapeutic strategies.

Pothu Usha Kiran, Jigar Haria, Reena Rani, Sudhir Singh

Abstract readReview
In one paragraph

Review in Tissue barriers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  3. Article
  4. Article
  5. Jujube Polysaccharide Promotes Neuroprotection and Longevity inInternational journal of molecular sciences · 2026
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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

4 authors.

Pothu Usha KiranDepartment of Biochemistry, TMMC&RC, Teerthanker Mahaveer University, Moradabad, India.ORCID 0009-0009-1021-5674
Jigar HariaDepartment of Medicine, TMMC&RC, Teerthanker Mahaveer University, Moradabad, India.
Reena RaniDepartment of Biochemistry, TMMC&RC, Teerthanker Mahaveer University, Moradabad, India.
Sudhir SinghDepartment of Microbiology, TMMC&RC, Teerthanker Mahaveer University, Moradabad, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by motor symptoms and progressive degeneration of dopaminergic neurons. Accumulating evidence indicates that mitochondrial dysfunction and oxidative stress are major contributors to PD pathogenesis.

objectivesThis review explores the molecular mechanisms underlying PD, emphasizing mitochondrial dysfunction and oxidative stress. It also examines genetic and environmental contributors, emerging biomarkers, and future treatment strategies.

methodsAn extensive literature review was conducted, focusing on mitochondrial biology, oxidative stress, genetic mutations, and environmental toxins relevant to PD. Investigations into treatment options - including redox therapies, gene therapies, and lifestyle approaches - were also examined.

resultsMitochondrial dysfunction in PD includes disrupted oxidative phosphorylation and elevated reactive oxygen species (ROS). This also affects calcium homeostasis, especially in substantia nigra neurons. Genetic mutations (PINK1, Parkin, DJ-1, LRRK2, GBA) impair mitophagy and antioxidant defenses. Environmental toxins (e.g. MPTP, rotenone) further damage mitochondrial function and contribute to dopaminergic neuron loss. Emerging biomarkers involve measurements of lipid peroxidation and mitochondrial DNA damage. Promising therapeutic strategies include mitochondria-targeted antioxidants (e.g. MitoQ), PINK1-based gene therapy, Parkin activation, ketogenic diet, and exercise-induced mitochondrial biogenesis.

conclusionsMitochondrial dysfunction and oxidative stress are central to PD pathophysiology. Strategies targeting these mechanisms may slow disease progression. Future research should emphasize combination therapies and early intervention trials, alongside biomarker integration, to enhance clinical outcomes.

Indexed as

BiomarkersMitochondriaOxidative StressParkinson DiseaseAnimalsHumansBiomarkersMitochondrial dysfunctionoxidative stressParkinson’s disease

Identifiers

PMID40813952
PMCPMC12962276

What OpenQuestion 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 OpenQuestion graph.