Evidence map›Paper›PMID 40163151›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.

Al-Hassan Soliman Wadan, Ahmed H Shaaban, Mohamed Z El-Sadek, Salah Abdelfatah Mostafa, Ahmed Sherief Moshref, Ahmed El-Hussein, Doha El-Sayed Ellakwa, Samah S Mehanny

Abstract readReview
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
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  11. Article
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  14. Mitochondrial CaBiomolecules · 2026
    Review
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  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.

Al-Hassan Soliman WadanDepartment of Oral Biology, Faculty of Dentistry, Galala University, Galala Plateau, Attaka, Suez Governorate, 15888, Egypt. Alhassan.soliman.168@gmail.com.
Ahmed H ShaabanDepartment of Biology, Faculty of Science, Galala University, Galala Plateau, Attaka,, Suez Governorate, 15888, Egypt.
Mohamed Z El-SadekDepartment of Biology, Faculty of Science, Galala University, Galala Plateau, Attaka,, Suez Governorate, 15888, Egypt.
Salah Abdelfatah MostafaBiotechnology Program, Faculty of Agriculture, Ain Shams University, Ain Shams, Egypt.
Ahmed Sherief MoshrefFaculty of Dentistry, Galala University, Galala Plateau, Attaka, Suez Governorate, 15888, Egypt.
Ahmed El-HusseinDepartment of Biology, Faculty of Science, Galala University, Galala Plateau, Attaka,, Suez Governorate, 15888, Egypt.
Doha El-Sayed EllakwaDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy for Girls, Al-Azhar University, Cairo, Egypt.
Samah S MehannyDepartment of Oral Biology, Faculty of Dentistry, Galala University, Galala Plateau, Attaka, Suez Governorate, 15888, Egypt.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative disorders present significant challenges to modern medicine because of their complex etiology, pathogenesis, and progressive nature, which complicate practical treatment approaches. Mitochondrial dysfunction is an important contributor to the pathophysiology of various neurodegenerative illnesses, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). This review paper examines the current literature highlighting the multifaceted functions of mitochondria, including energy production, calcium signaling, apoptosis regulation, mitochondrial biogenesis, mitochondrial dynamics, axonal transport, endoplasmic reticulum-mitochondrial interactions, mitophagy, mitochondrial proteostasis, and their crucial involvement in neuronal health. The literature emphasizes the increasing recognition of mitochondrial dysfunction as a critical factor in the progression of neurodegenerative disorders, marking a shift from traditional symptom management to innovative mitochondrial-based therapies. By discussing mitochondrial mechanisms, including mitochondrial quality control (MQC) processes and the impact of oxidative stress, this review highlights the need for novel therapeutic strategies to restore mitochondrial function, protect neuronal connections and integrity, and slow disease progression. This comprehensive review aims to provide insights into potential interventions that could transform the treatment landscape for neurodegenerative diseases, addressing symptoms and underlying pathophysiological changes.

Indexed as

MitochondriaNeurodegenerative DiseasesAnimalsHumansOxidative StressMitochondria-focused therapiesMitochondrial dysfunctionNeurodegenerative diseasesOxidative stressTherapeutic strategies

Identifiers

PMID40163151
PMCPMC12449425

What OpenQuestion holds

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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.