ArticleNeural regeneration research2023
Altered O-GlcNAcylation and mitochondrial dysfunction, a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis 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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Role of O-GlcNAcylation in Central Nervous System Development and Injuries: A Systematic Review.Molecular neurobiology · 2024Pooled it
- PCSK9 in bridging metabolism and neurodegeneration: a new paradigm for alzheimer's treatment.Metabolic brain disease · 2026Review
- Protein lactylation in Alzheimer's disease: bridging metabolism, pathology, and therapeutic opportunity.Frontiers in aging neuroscience · 2026Review
- Unlocking the Sugar Code: Implications and Consequences of Glycosylation in Alzheimer's Disease and Other Tauopathies.Biomedicines · 2025Review
- The CSF Levels of Mitochondrial Phosphoenolpyruvate Carboxykinase 2 as a Novel Biomarker in Alzheimer's Disease.Molecular neurobiology · 2025Article
- Tirzepatide: a novel therapeutic approach for Alzheimer's disease.Metabolic brain disease · 2025Review
- Roles of Lysine Methylation in Glucose and Lipid Metabolism: Functions, Regulatory Mechanisms, and Therapeutic Implications.Biomolecules · 2024Review
- Hypoglycemia and Alzheimer Disease Risk: The Possible Role of Dasiglucagon.Cellular and molecular neurobiology · 2024Review
- Mitochondria in Alzheimer's Disease Pathogenesis.Life (Basel, Switzerland) · 2024Review
- Investigation of Pancreatic-beta Cells Role in the Biological Process of Ageing.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Low glucose induced Alzheimer's disease-like biochemical changes in human induced pluripotent stem cell-derived neurons is due to dysregulated O-GlcNAcylation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Multifaceted roles of mitochondrial dysfunction in diseases: from powerhouses to saboteurs.Archives of pharmacal research · 2023Review
- Roles of protein post-translational modifications in glucose and lipid metabolism: mechanisms and perspectives.Molecular medicine (Cambridge, Mass.) · 2023Review
- Chemical Biology Approaches to Understanding Neuronal O-GlcNAcylation.Israel journal of chemistry · 2023Article
- O-GlcNAcylation is crucial for sympathetic neuron development, maintenance, functionality and contributes to peripheral neuropathy.Frontiers in neuroscience · 2023Article
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
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease is a neurodegenerative disease that affected over 6.5 million people in the United States in 2021, with this number expected to double in the next 40 years without any sort of treatment. Due to its heterogeneity and complexity, the etiology of Alzheimer's disease, especially sporadic Alzheimer's disease, remains largely unclear. Compelling evidence suggests that brain glucose hypometabolism, preceding Alzheimer's disease hallmarks, is involved in the pathogenesis of Alzheimer's disease. Herein, we discuss the potential causes of reduced glucose uptake and the mechanisms underlying glucose hypometabolism and Alzheimer's disease pathology. Specifically, decreased O-GlcNAcylation levels by glucose deficiency alter mitochondrial functions and together contribute to Alzheimer's disease pathogenesis. One major problem with Alzheimer's disease research is that the disease progresses for several years before the onset of any symptoms, suggesting the critical need for appropriate models to study the molecular changes in the early phase of Alzheimer's disease progression. Therefore, this review also discusses current available sporadic Alzheimer's disease models induced by metabolic abnormalities and provides novel directions for establishing a human neuronal sporadic Alzheimer's disease model that better represents human sporadic Alzheimer's disease as a metabolic disease.
Indexed as
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.