ArticleMolecular neurobiology2020
GLUT12 Expression in Brain of Mouse Models of Alzheimer's Disease.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- Bibliometric Analysis Study on the Mechanisms of Brain Energy Metabolism Disorders in Alzheimer's Disease From 2000 to 2020.Frontiers in neurology · 2021Pooled it
- A Systematic Review of Glucose Transport Alterations in Alzheimer's Disease.Frontiers in neuroscience · 2021Pooled it
- Sex differences in brain glucose metabolism and Alzheimer's disease risk and progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Insights into insulin signalling and oxidative stress in the Tg2576 mouse model of familial Alzheimer's disease: effects of chronic oral galactose administration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Human Glucose Transporters in Health and Selected Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- The glucose transporter GLUT12, a new actor in obesity and cancer.Journal of physiology and biochemistry · 2025Review
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Dysregulation of energy metabolism in Alzheimer's disease.Journal of neurology · 2024Review
- Royal jelly a promising therapeutic intervention and functional food supplement: A systematic review.Heliyon · 2024Review
- Cellular and molecular mechanisms of the blood-brain barrier dysfunction in neurodegenerative diseases.Fluids and barriers of the CNS · 2024Review
- A genome-wide association study of Chinese and English language phenotypes in Hong Kong Chinese children.NPJ science of learning · 2024Article
- Bridging the gap: glucose transporters, Alzheimer's, and future therapeutic prospects.Frontiers in cell and developmental biology · 2024Review
- Brain Metabolic Alterations in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Punicic Acid and Its Role in the Prevention of Neurological Disorders: A Review.Foods (Basel, Switzerland) · 2022Review
- Disruption of Glucose Metabolism in AgedFrontiers in integrative neuroscience · 2021Article
- Glucose, Fructose, and Urate Transporters in the Choroid Plexus Epithelium.International journal of molecular sciences · 2020Review
- Royal Jelly as an Intelligent Anti-Aging Agent-A Focus on Cognitive Aging and Alzheimer's Disease: A Review.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The brain depends on glucose as a source of energy. This implies the presence of glucose transporters, being GLUT1 and GLUT3 the most relevant. Expression of GLUT12 is found in mouse and human brain at low levels. We previously demonstrated GLUT12 upregulation in the frontal cortex of aged subjects that was even higher in aged Alzheimer's disease (AD) patients. However, the cause and the mechanism through which this increase occurs are still unknown. Here, we aimed to investigate whether the upregulation of GLUT12 in AD is related with aging or Aβ deposition in comparison with GLUT1, GLUT3, and GLUT4. In the frontal cortex of two amyloidogenic mouse models (Tg2576 and APP/PS1) GLUT12 levels were increased. Contrary, expression of GLUT1 and GLUT3 were decreased, while GLUT4 did not change. In aged mice and the senescence-accelerated model SAMP8, GLUT12 and GLUT4 were upregulated in comparison with young animals. GLUT1 and GLUT3 did not show significant changes with age. The effect of β-amyloid (Aβ) deposition was also evaluated in Aβ peptide i.c.v. injected mice. In the hippocampus, GLUT12 expression increased whereas GLUT4 was not modified. Consistent with the results in the amyloidogenic models, GLUT3 and GLUT1 were downregulated. In summary, Aβ increases GLUT12 protein expression in the brain pointing out a central role of the transporter in AD pathology and opening new perspectives for the treatment of this neurodegenerative disease.
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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.