ReviewJournal of neuroscience research2007
Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders.
Review in Journal of neuroscience research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 111 citations in OpenAlex.
- Loss of Ezrin triggers mitochondrial dysfunction and oxidative stress, associated with neuronal cell death.Cell death discovery · 2025Article
- Comprehensive Metabolomic Profiling and Biological Activity Analysis ofFood science & nutrition · 2025Article
- Visualizing fatigue mechanisms in non-communicable diseases: an integrative approach with multi-omics and machine learning.BMC medical informatics and decision making · 2025Article
- Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Tissue Hypoxia and Associated Innate Immune Factors in Experimental Autoimmune Optic Neuritis.International journal of molecular sciences · 2024Article
- ACO2 deficiency increases vulnerability to Parkinson's disease via dysregulating mitochondrial function and histone acetylation-mediated transcription of autophagy genes.Communications biology · 2023Article
- Posttreatment with Ospemifene Attenuates Hypoxia- and Ischemia-Induced Apoptosis in Primary Neuronal Cells via Selective Modulation of Estrogen Receptors.Neurotoxicity research · 2023Article
- Hydrogen Ion Dynamics as the Fundamental Link between Neurodegenerative Diseases and Cancer: Its Application to the Therapeutics of Neurodegenerative Diseases with Special Emphasis on Multiple Sclerosis.International journal of molecular sciences · 2022Review
- Mitochondrial dysfunction in perinatal asphyxia: role in pathogenesis and potential therapeutic interventions.Molecular and cellular biochemistry · 2021Review
- Contrasting Metabolic Insufficiency in Aging and Dementia.Aging and disease · 2021Review
- High-Resolution Metabolomic Assessment of Pesticide Exposure in Central Valley, California.Chemical research in toxicology · 2021Article
- Novel Neuroprotective Potential of Crocin in Neurodegenerative Disorders: An Illustrated Mechanistic Review.Neurochemical research · 2020Review
- Postnatal growth retardation is associated with intestinal mucosa mitochondrial dysfunction and aberrant energy status in piglets.Journal of cellular and molecular medicine · 2020Article
- Intracellular monitoring of NADH release from mitochondria using a single functionalized nanowire electrode.Chemical science · 2020Article
- Neuroimmunomodulation by estrogen in health and disease.AIMS neuroscience · 2020Review
- Lipidomics Detection of Brain Cardiolipins in Plasma Is Associated With Outcome After Cardiac Arrest.Critical care medicine · 2019Observational
- Article
- Mitochondrial Dysfunction in Neural Injury.Frontiers in neuroscience · 2019Review
- The regulator of calcineurin 1 increases adenine nucleotide translocator 1 and leads to mitochondrial dysfunctions.Journal of neurochemistry · 2017Article
- Pre-B-cell colony-enhancing factor protects against apoptotic neuronal death and mitochondrial damage in ischemia.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson's and Huntington's diseases. Although much evidence supports that the electron transport chain dysfunction in these metabolic abnormalities has both genetic and intracellular environmental causes, alternative mechanisms are being explored. These include direct, reversible inhibition of cytochrome oxidase by nitric oxide, release of mitochondrial cytochrome c, oxidative inhibition of mitochondrial matrix dehydrogenases and adenine nucleotide transport, the availability of NAD for dehydrogenase reactions, respiratory uncoupling by activities such as that of the permeability transition pore, and altered mitochondrial structure and intracellular trafficking. This review focuses on the catabolism of neuronal NAD and the release of neuronal mitochondrial NAD as important contributors to metabolic dysfunction. In addition, the relationship between apoptotic signaling cascades and disruption of mitochondrial energy metabolism is considered in light of the fine balance between apoptotic and necrotic neural cell death.
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Identifiers
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.