ReviewOxidative medicine and cellular longevity2015
Mitochondria-Targeted Protective Compounds in Parkinson's and Alzheimer's Diseases.
Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
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
41 citing papers in PubMed, 93 citations in OpenAlex.
- Targeting mitochondria for the treatment of neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- Multi-Target Neuroprotective Effects of Flavonoid-RichInternational journal of molecular sciences · 2025Article
- The Mitochondrial-Astrocyte-Neuron Triad Hypothesis in Parkinson's Disease: A Toxic Feedback Loop of Metabolism, Aggregation, and Oxidative Stress.Neurochemical research · 2025Review
- Transcriptomics, single-cell sequencing and spatial sequencing-based studies of cerebral ischemia.European journal of medical research · 2025Review
- Therapeutic Expedition of Luteolin against Brain-related Disorders: An Updated Review.Combinatorial chemistry & high throughput screening · 2025Review
- A High-Throughput Screening of a Natural Products Library for Mitochondria Modulators.Biomolecules · 2024Article
- Pathological and Therapeutic Advances in Parkinson's Disease: Mitochondria in the Interplay.Journal of Alzheimer's disease : JAD · 2023Review
- Peanut (Arachis hypogaea) sprout prevents high-fat diet-induced cognitive impairment by improving mitochondrial function.Scientific reports · 2022Article
- Modulation of Cellular Circadian Rhythms by Secondary Metabolites of Lichens.Frontiers in cellular neuroscience · 2022Article
- 1,5-Benzodiazepin-2(3H)-ones: In Vitro Evaluation as Antiparkinsonian Agents.Antioxidants (Basel, Switzerland) · 2021Article
- Healthy dietary intake moderates the effects of age on brain iron concentration and working memory performance.Neurobiology of aging · 2021Article
- Pyrroloquinoline quinone promotes mitochondrial biogenesis in rotenone-induced Parkinson's disease model via AMPK activation.Acta pharmacologica Sinica · 2021Article
- The mechanism and prevention of mitochondrial injury after exercise.Journal of physiology and biochemistry · 2021Review
- Claulansine F-Donepezil Hybrids as Anti-Alzheimer's Disease Agents with Cholinergic, Free-Radical Scavenging, and Neuroprotective Activities.Molecules (Basel, Switzerland) · 2021Article
- Protective Effects of Silymarin Against D-Gal/LPS-Induced Organ Damage and Inflammation in Mice.Drug design, development and therapy · 2021Article
- Mitochondrial Transplantation Attenuates Cerebral Ischemia-Reperfusion Injury: Possible Involvement of Mitochondrial Component Separation.Oxidative medicine and cellular longevity · 2021Article
- Neuroprotective Activities ofMolecules (Basel, Switzerland) · 2020Article
- A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.Aging and disease · 2020Review
- Miro, a Rho GTPase genetically interacts with Alzheimer's disease-associated genes (Biology open · 2020Article
- Dl-3-n-butylphthalide attenuates mouse behavioral deficits to chronic social defeat stress by regulating energy metabolism via AKT/CREB signaling pathway.Translational psychiatry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are cytoplasmic organelles that regulate both metabolic and apoptotic signaling pathways; their most highlighted functions include cellular energy generation in the form of adenosine triphosphate (ATP), regulation of cellular calcium homeostasis, balance between ROS production and detoxification, mediation of apoptosis cell death, and synthesis and metabolism of various key molecules. Consistent evidence suggests that mitochondrial failure is associated with early events in the pathogenesis of ageing-related neurodegenerative disorders including Parkinson's disease and Alzheimer's disease. Mitochondria-targeted protective compounds that prevent or minimize mitochondrial dysfunction constitute potential therapeutic strategies in the prevention and treatment of these central nervous system diseases. This paper provides an overview of the involvement of mitochondrial dysfunction in Parkinson's and Alzheimer's diseases, with particular attention to in vitro and in vivo studies on promising endogenous and exogenous mitochondria-targeted protective compounds.
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What OpenQuestion holds
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.