ReviewMolecular neurobiology2003
Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria.
Review in Molecular neurobiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 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
178 citing papers in PubMed, 2 syntheses or guidelines pooled it, 456 citations in OpenAlex.
- Pooled it
- Nanotechnology-based drug delivery systems for the treatment of Alzheimer's disease.International journal of nanomedicine · 2015Pooled it
- Molecular Editing Reveals a Bilobalide Chemotype that Attenuates Prolyl Endopeptidase (PREP)-Linked Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phytochemicals with potential NMDAR-inhibitory activities: a review of neuroprotective mechanisms against excitotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026Review
- Is there a link between multiple sclerosis and Alzheimer disease? A critical note.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Association between Toxoplasma gondii seropositivity and Alzheimer's disease: a case-control study.Parasitology research · 2026Article
- Beyond biochemical cascades: novel bio-mechanical and epigenetic paradigms of glial SASP in brain aging.Metabolic brain disease · 2026Review
- HIV Infection, Neurotoxicity, Inflammation, Premature Aging, and Therapeutic Challenges to PLWH: An Overview.International journal of molecular sciences · 2026Review
- Oral Dysbiosis and Neuroinflammation: Implications for Alzheimer's, Parkinson's and Mood Disorders.Microorganisms · 2026Review
- Early α-Synuclein Pathology Induces Neuroinflammation and Decreases Topoisomerase IIβ Expression in A53T Mice.Inflammation · 2025Article
- Neuronal regulated cell death in aging-related neurodegenerative diseases: key pathways and therapeutic potentials.Neural regeneration research · 2025Article
- Post-COVID Condition and Neuroinflammation: Possible Management with Antioxidants.Antioxidants (Basel, Switzerland) · 2025Review
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- Escitalopram alters tryptophan metabolism, plasma lipopolysaccharide, and the inferred functional potential of the gut microbiome in deer mice showing compulsive-like rigidity.Acta neuropsychiatrica · 2025Article
- Skeletal muscle innervation: Reactive oxygen species as regulators of neuromuscular junction dynamics and motor unit remodeling.Free radical biology & medicine · 2025Review
- NMDA receptors in neurodegenerative diseases: mechanisms and emerging therapeutic strategies.Frontiers in aging neuroscience · 2025Review
- Oxidative stress and mitochondrial dysfunction contributes to postoperative cognitive dysfunction in elderly rats dependent on NLRP3 activation.Metabolic brain disease · 2024Article
- Oxidative stress-mediated neuroinflammation in Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- The potential role of nitric oxide in the anticonvulsant effects of betulin in pentylenetetrazole (PTZ)-induced seizures in mice.IBRO neuroscience reports · 2024Article
- Current biomarkers and treatment strategies in Alzheimer disease: An overview and future perspectives.IBRO neuroscience reports · 2024Review
118 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In inflammatory, infectious, ischemic, and neurodegenerative pathologies of the central nervous system (CNS) glia become "activated" by inflammatory mediators, and express new proteins such as the inducible isoform of nitric oxide synthase (iNOS). Although these activated glia have benefi- cial roles, in vitro they potently kill cocultured neurons, and there is increasing evidence that they contribute to pathology in vivo. Nitric oxide (NO) from iNOS appears to be a key mediator of such glial-induced neuronal death. The high sensitivity of neurons to NO is partly due to NO causing inhibition of respiration, rapid glutamate release from both astrocytes and neurons, and subsequent excitotoxic death of the neurons. NO is a potent inhibitor of mitochondrial respiration, due to reversible binding of NO to cytochrome oxidase in competition with oxygen, resulting in inhibition of energy production and sensitization to hypoxia. Activated astrocytes or microglia cause a potent inhibition of respiration in cocultured neurons due to glial NO inhibiting cytochrome oxidase within the neurons, resulting in ATP depletion and glutamate release. In some conditions, glutamate- induced neuronal death can itself be mediated by N-methyl-D-aspartate (NMDA)-receptor activation of the neuronal isoform of NO synthase (nNOS) causing mitochondrial damage. In addition NO can be converted to a number of reactive derivatives such as peroxynitrite, NO2, N2O3, and S-nitrosothiols that can kill cells in part by inhibiting mitochondrial respiration or activation of mitochondrial permeability transition, triggering neuronal apoptosis or necrosis.
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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.