ArticleOxidative medicine and cellular longevity2019
Suppression of Alzheimer's Disease-Like Pathology Progression by Mitochondria-Targeted Antioxidant SkQ1: A Transcriptome Profiling Study.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Transcriptome graph transformer: a graph transformer-based unsupervised model for transcriptome data analysis.BMC bioinformatics · 2026Article
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- Mitochondrial ecosystem restoration in Alzheimer's disease: from mechanisms to multi-target therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
- Autophagy deficiency exacerbates iron overload induced reactive oxygen species production and apoptotic cell death in skeletal muscle cells.Cell death & disease · 2023Article
- The Rat Brain Transcriptome: From Infancy to Aging and Sporadic Alzheimer's Disease-like Pathology.International journal of molecular sciences · 2023Article
- Altered Mitochondrial Morphology and Bioenergetics in a New Yeast Model Expressing Aβ42.International journal of molecular sciences · 2023Article
- Calorie Restriction Provides Kidney Ischemic Tolerance in Senescence-Accelerated OXYS Rats.International journal of molecular sciences · 2022Article
- The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence.Antioxidants (Basel, Switzerland) · 2022Review
- Targeting whole body metabolism and mitochondrial bioenergetics in the drug development for Alzheimer's disease.Acta pharmaceutica Sinica. B · 2022Review
- Changes in Glial Support of the Hippocampus during the Development of an Alzheimer's Disease-like Pathology and Their Correction by Mitochondria-Targeted Antioxidant SkQ1.International journal of molecular sciences · 2022Article
- Discovery of Novel Drug Candidates for Alzheimer's Disease by Molecular Network Modeling.Frontiers in aging neuroscience · 2022Article
- Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- ATP Synthase and Mitochondrial Bioenergetics Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- MEK1/2-ERK Pathway Alterations as a Therapeutic Target in Sporadic Alzheimer's Disease: A Study in Senescence-Accelerated OXYS Rats.Antioxidants (Basel, Switzerland) · 2021Article
- Early onset senescence and cognitive impairment in a murine model of repeated mTBI.Acta neuropathologica communications · 2021Article
- Therapeutic Approaches to Treat Mitochondrial Diseases: "One-Size-Fits-All" and "Precision Medicine" Strategies.Pharmaceutics · 2020Review
- Neuroprotective effects of Fomes officinalis Ames polysaccharides on AβCytotechnology · 2020Article
- SkQ1 Suppresses the p38 MAPK Signaling Pathway Involved in Alzheimer's Disease-Like Pathology in OXYS Rats.Antioxidants (Basel, Switzerland) · 2020Article
- Metabolic dysfunction and mitochondrial failure in Alzheimer's disease: integrating pathophysiology, clinical evidence and emerging interventions.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common type of dementia, with increasing prevalence and no disease-modifying treatment available yet. There is increasing evidence-from interventions targeting mitochondria-that may shed some light on new strategies for the treatment of AD. Previously, using senescence-accelerated OXYS rats that simulate key characteristics of sporadic AD, we have shown that treatment with mitochondria-targeted antioxidant SkQ1 (plastoquinonyl-decyltriphenylphosphonium) from age 12 to 18 months (that is, during active progression of AD-like pathology)-via improvement of mitochondrial function-prevented the neuronal loss and synaptic damage, enhanced neurotrophic supply, and decreased amyloid-
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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.