ReviewOxidative medicine and cellular longevity2014
Mitochondrial dysfunction: different routes to Alzheimer's disease therapy.
Review in Oxidative medicine and cellular longevity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 207 citations in OpenAlex.
- Pharmacological approaches to enhance mitochondrial biogenesis: focus on PGC-1Α, AMPK, and SIRT1 in cellular health.Molecular biology reports · 2025Pooled it
- Multivariate meta-analyses of mitochondrial complex I and IV in major depressive disorder, bipolar disorder, schizophrenia, Alzheimer disease, and Parkinson disease.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Pooled it
- Mitochondria-Targeted Nanotherapeutics: A Promising Strategy in Modulating Mitochondrial Function, Transfer, and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Vocal Fold Atrophy in an Alzheimer's Disease Rat Model.The Laryngoscope · 2026Article
- Physical Exercise Counteracts Impaired Cognition by Improving Mitochondrial Function.International journal of molecular sciences · 2026Review
- Roles of Reactive Oxygen Species in Relationships Between Viral Infections and Alzheimer's Disease and Related Dementia.Antioxidants (Basel, Switzerland) · 2026Review
- Bioinformatics insights into mitochondrial and immune gene regulation in Alzheimer's disease.European journal of medical research · 2025Article
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- A novelBiology methods & protocols · 2025Article
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
- Alzheimer's Disease: Exploring the Landscape of Cognitive Decline.ACS chemical neuroscience · 2024Review
- Review
- New Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses.Aging and disease · 2024Review
- Microneedles: A Versatile Drug Delivery Carrier for Phytobioactive Compounds as a Therapeutic Modulator for Targeting Mitochondrial Dysfunction in the Management of Neurodegenerative Diseases.Current neuropharmacology · 2024Review
- Mitochondrial Inherited Disorders and their Correlation with Neurodegenerative Diseases.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Advances in the Study of the Pathology and Treatment of Alzheimer's Disease and Its Association with Periodontitis.Life (Basel, Switzerland) · 2023Review
- Mechanistic multiscale modelling of energy metabolism in human astrocytes reveals the impact of morphology changes in Alzheimer's Disease.PLoS computational biology · 2023Article
- Review
- Neuroprotective and Antioxidant Role of Oxotremorine-M, a Non-selective Muscarinic Acetylcholine Receptors Agonist, in a Cellular Model of Alzheimer Disease.Cellular and molecular neurobiology · 2023Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are dynamic ATP-generating organelle which contribute to many cellular functions including bioenergetics processes, intracellular calcium regulation, alteration of reduction-oxidation potential of cells, free radical scavenging, and activation of caspase mediated cell death. Mitochondrial functions can be negatively affected by amyloid β peptide (Aβ), an important component in Alzheimer's disease (AD) pathogenesis, and Aβ can interact with mitochondria and cause mitochondrial dysfunction. One of the most accepted hypotheses for AD onset implicates that mitochondrial dysfunction and oxidative stress are one of the primary events in the insurgence of the pathology. Here, we examine structural and functional mitochondrial changes in presence of Aβ. In particular we review data concerning Aβ import into mitochondrion and its involvement in mitochondrial oxidative stress, bioenergetics, biogenesis, trafficking, mitochondrial permeability transition pore (mPTP) formation, and mitochondrial protein interaction. Moreover, the development of AD therapy targeting mitochondria is also discussed.
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Registered trials
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.