ArticleNeurotoxicity research2009
Nitric oxide as an initiator of brain lesions during the development of Alzheimer disease.
Article in Neurotoxicity research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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.
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Who cites it
27 citing papers in PubMed, 112 citations in OpenAlex.
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- Are current etiological theories of Alzheimer's disease falsifiable? An epistemological assessment.Frontiers in aging neuroscience · 2025Article
- A common molecular and cellular pathway in developing Alzheimer and cancer.Biochemistry and biophysics reports · 2024Review
- Therapeutic potential of berries in age-related neurological disorders.Frontiers in pharmacology · 2024Review
- A Scoping Review of Alzheimers Disease Hypotheses: An Array of Uni- and Multi-Factorial Theories.Journal of Alzheimer's disease : JAD · 2024Article
- Analysis of endothelial gene polymorphisms in Spanish patients with vascular dementia and Alzheimer´s disease.Scientific reports · 2023Article
- Nitric Oxide/Nitric Oxide Synthase System in the Pathogenesis of Neurodegenerative Disorders-An Overview.Antioxidants (Basel, Switzerland) · 2023Review
- Natural Product Co-Metabolism and the Microbiota-Gut-Brain Axis in Age-Related Diseases.Life (Basel, Switzerland) · 2022Review
- Intersection between Redox Homeostasis and Autophagy: Valuable Insights into Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- A metabolomic approach to identifying biomarkers in blood of Alzheimer's disease.Annals of clinical and translational neurology · 2019Article
- The Effects of Flavonoids on Cardiovascular Health: A Review of Human Intervention Trials and Implications for Cerebrovascular Function.Nutrients · 2018Review
- Altered plasma arginine metabolome precedes behavioural and brain arginine metabolomic profile changes in the APPswe/PS1ΔE9 mouse model of Alzheimer's disease.Translational psychiatry · 2018Article
- Plasma microparticles in Alzheimer's disease: The role of vascular dysfunction.Metabolic brain disease · 2018Article
- Phytochemical investigations and antioxidant potential of roots of Leea macrophylla (Roxb.).BMC research notes · 2017Article
- Reversing synapse loss in Alzheimer's disease: Rho-guanosine triphosphatases and insights from other brain disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015Review
- Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's Disease?Journal of Alzheimer's disease : JAD · 2015Review
- Vascular dysfunction associated with type 2 diabetes and Alzheimer's disease: a potential etiological linkage.Medical science monitor basic research · 2014Review
- Antifungal and antioxidant activity of Crassocephalum bauchiense (Hutch.) Milne-Redh ethyl acetate extract and fractions (Asteraceae).BMC research notes · 2014Article
- The interplay between iron accumulation, mitochondrial dysfunction, and inflammation during the execution step of neurodegenerative disorders.Frontiers in pharmacology · 2014Review
- Nitric oxide donors as neuroprotective agents after an ischemic stroke-related inflammatory reaction.Oxidative medicine and cellular longevity · 2013Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) is an important regulatory molecule for the host defense that plays a fundamental role in the cardiovascular, immune, and nervous systems. NO is synthesized through the conversion of L-arginine to L-citrulline by the enzyme NO synthase (NOS), which is found in three isoforms classified as neuronal (nNOS), inducible (iNOS), and endothelial (eNOS). Recent evidence supports the theory that this bioactive molecule has an influential role in the disruption of normal brain and vascular homeostasis, a condition known to elucidate chronic hypoperfusion which ultimately causes the development of brain lesions and the pathology that typify Alzheimer disease (AD). In addition, vascular NO activity appears to be a major contributor to this pathology before any overexpression of NOS isoforms is observed in the neuron, glia, and microglia of the brain tree, where the overexpression the NOS isoforms causes the formation of a large amount of NO. We hypothesize that since an imbalance between the NOS isoforms and endothelin-1 (ET-1), a human gene that encodes for blood vessel constriction, can cause antioxidant system insufficiency; by using pharmacological intervention with NO donors and/or NO suppressors, the brain lesions and the downstream progression of brain pathology and dementia in AD should be delayed or minimized.
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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.