ArticleScientific reports2016
Elevation of brain glucose and polyol-pathway intermediates with accompanying brain-copper deficiency in patients with Alzheimer's disease: metabolic basis for dementia.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Are high copper levels related to Alzheimer's and Parkinson's diseases? A systematic review and meta-analysis of articles published between 2011 and 2022.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Pooled it
- A high-glycemic diet is associated with cerebral amyloid burden in cognitively normal older adults.The American journal of clinical nutrition · 2017Trial
- Spatiotemporal heterogeneity and dynamic evolution of microglial glucose metabolic reprogramming in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Polyol pathway dysregulation in CSF links glucose metabolism to tau pathology independently of amyloid and genetic predisposition.medRxiv : the preprint server for health sciences · 2026Article
- Fructose: metabolic signal and modern hazard.Nature metabolism · 2026Review
- Article
- Anesthesia, perimortem conditions, and brain harvest method govern the measured metabolome: analysis of substandard samples generates flawed metabolite levels.Oxford open neuroscience · 2026Article
- High glucose induces hippocampal neuron impairment through the SKP1/COX7C pathway: A potential mechanism for perimenopausal depression.Acta pharmaceutica Sinica. B · 2025Article
- Metabolites associated with type 2 diabetes and Alzheimer's disease trigger differential intracellular signaling responses in mouse primary neurons.Brain research · 2025Article
- Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities.Molecular neurodegeneration · 2025Review
- Do microglia metabolize fructose in Alzheimer's disease?Journal of neuroinflammation · 2025Review
- Differential responses of primary neuron-secreted MCP-1 and IL-9 to type 2 diabetes and Alzheimer's disease-associated metabolites.Scientific reports · 2024Article
- Untargeted Metabolomic Profiling Reveals Differentially Expressed Serum Metabolites and Pathways in Type 2 Diabetes Patients with and without Cognitive Decline: A Cross-Sectional Study.International journal of molecular sciences · 2024Article
- Metabolic profiles associated with exposure to ambient particulate air pollution: findings from the Betula cohort.Frontiers in public health · 2024Article
- Brain insulin resistance and Alzheimer's disease: a systematic review.Dementia & neuropsychologia · 2024Review
- Fructose-mediated AGE-RAGE axis: approaches for mild modulation.Frontiers in nutrition · 2024Review
- Differential responses of primary neuron-secreted MCP-1 and IL-9 to type 2 diabetes and Alzheimer's disease-associated metabolites.bioRxiv : the preprint server for biology · 2023Article
- The Connection between Chronic Liver Damage and Sporadic Alzheimer's Disease: Evidence and Insights from a Rat Model.Brain sciences · 2023Article
- Sorbitol reduction via govorestat ameliorates synaptic dysfunction and neurodegeneration in sorbitol dehydrogenase deficiency.JCI insight · 2023Article
- Multi-regional alterations in glucose and purine metabolic pathways in the Parkinson's disease dementia brain.NPJ Parkinson's disease · 2023Article
Corrections and comments
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Authors and funding
25 authors at 6 institutions in 3 countries.
Funding
Abstract
Impairment of brain-glucose uptake and brain-copper regulation occurs in Alzheimer's disease (AD). Here we sought to further elucidate the processes that cause neurodegeneration in AD by measuring levels of metabolites and metals in brain regions that undergo different degrees of damage. We employed mass spectrometry (MS) to measure metabolites and metals in seven post-mortem brain regions of nine AD patients and nine controls, and plasma-glucose and plasma-copper levels in an ante-mortem case-control study. Glucose, sorbitol and fructose were markedly elevated in all AD brain regions, whereas copper was correspondingly deficient throughout (all P < 0.0001). In the ante-mortem case-control study, by contrast, plasma-glucose and plasma-copper levels did not differ between patients and controls. There were pervasive defects in regulation of glucose and copper in AD brain but no evidence for corresponding systemic abnormalities in plasma. Elevation of brain glucose and deficient brain copper potentially contribute to the pathogenesis of neurodegeneration in AD.
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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.