ReviewNature reviews. Neuroscience2019
Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease.
Review in Nature reviews. Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,030 papers, 3 of them syntheses that pooled it.
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
1,030 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,796 citations in OpenAlex.
- Lactate Changes Quantified by fMRS: A Meta-Analysis.NMR in biomedicine · 2026Pooled it
- Anti-neuroinflammatory and neuroprotective effects of acteoside (verbascoside) in experimental models of neurodegeneration: a systematic review and meta-analysis.Inflammopharmacology · 2026Pooled it
- Biomarkers and pathways in autism spectrum disorder: An individual meta-analysis based on proteomic and metabolomic data.European archives of psychiatry and clinical neuroscience · 2025Pooled it
- Article
- Oxidative stress biomarkers and flavonoids in Alzheimer's disease: current clinical evidence and therapeutic perspectives.Redox report : communications in free radical research · 2026Review
- Tannic Acid Mitigates Monosodium Glutamate-Induced Cortical Damage by Modulating Synaptic and Calcium-Related Gene and Protein Expression.Journal of applied toxicology : JAT · 2026Article
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Thalamic Nuclei Atrophy in Type 1 Diabetes Mellitus Across Disease Duration.Journal of magnetic resonance imaging : JMRI · 2026Article
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- A multi-omics and machine-learning framework reveals shared druggable targets for Alzheimer's disease and periodontitis and identifies amentoflavone and taraxerone as potential dual-action natural products.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Oxidative Stress and Its Mitigation in Neurodegenerative Disorders.Antioxidants (Basel, Switzerland) · 2026Article
- Reframing Alzheimer's Disease Through a Redox-Metabolic Framework.International journal of molecular sciences · 2026Review
- Dietary Patterns, Micronutrient Adequacy, and Metabolic Vulnerability in Alzheimer's Disease: A Critical Narrative Review.Nutrients · 2026Review
- Olfactory-Cleft Biopsy in Alzheimer's Disease: An Emerging Neuroimmune Window into Preclinical Pathobiology.International journal of molecular sciences · 2026Review
- Review
- Elucidating shared genetic signals between type 2 diabetes and three neurodegenerative dementia phenotypes.HGG advances · 2026Article
- Reduced expression of Brain Expressed X-linked genes in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- Article
- Neuroinflammatory and molecular pathways in Alzheimer's disease: mechanistic crosstalk and emerging therapeutic opportunities.Inflammopharmacology · 2026Review
- Hepatic-targeted low-intensity pulsed ultrasound attenuates cerebral amyloidosis via upregulating insulin-degrading enzyme.Metabolic brain disease · 2026Article
970 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 2 institutions in 2 countries.
Funding
Abstract
Alzheimer disease (AD) is a major cause of age-related dementia. We do not fully understand AD aetiology and pathogenesis, but oxidative damage is a key component. The brain mostly uses glucose for energy, but in AD and amnestic mild cognitive impairment glucose metabolism is dramatically decreased, probably owing, at least in part, to oxidative damage to enzymes involved in glycolysis, the tricarboxylic acid cycle and ATP biosynthesis. Consequently, ATP-requiring processes for cognitive function are impaired, and synaptic dysfunction and neuronal death result, with ensuing thinning of key brain areas. We summarize current research on the interplay and sequence of these processes and suggest potential pharmacological interventions to retard AD progression.
Indexed as
Identifiers
What Socratic 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 Socratic graph.