ArticleNeurobiology of aging2014
Mammalian target of rapamycin hyperactivity mediates the detrimental effects of a high sucrose diet on Alzheimer's disease pathology.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- A randomized placebo-controlled trial of nicotinamide riboside in older adults with mild cognitive impairment.GeroScience · 2024Trial
- The impact of high-sugar diets on central nervous system disorders: mechanisms, pathogenesis, and dietary implication.Annals of medicine · 2025Review
- RNA methylation modifications in neurodegenerative diseases: Focus on their enzyme system.Journal of advanced research · 2025Review
- Identifying Links between Alzheimer's Disease and Type 2 Diabetes through Proteomics.Journal of proteome research · 2025Review
- Nutrition: A non-negligible factor in the pathogenesis and treatment of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?Antioxidants (Basel, Switzerland) · 2025Review
- A pathophysiological intersection between metabolic biomarkers and memory: a longitudinal study in the STZ-induced diabetic mouse model.Frontiers in physiology · 2025Article
- Ovariectomy and High Fat-Sugar-Salt Diet Induced Alzheimer's Disease/Vascular Dementia Features in Mice.Aging and disease · 2024Article
- Investigating CR1 as an indicated Gene for mild cognitive impairment in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2024Article
- Nutrients and Dementia: Prospective Study.Nutrients · 2023Article
- High Glycemia and Soluble Epoxide Hydrolase in Females: Differential Multiomics in Murine Brain Microvasculature.International journal of molecular sciences · 2022Article
- Feeding the Brain: Effect of Nutrients on Cognition, Synaptic Function, and AMPA Receptors.Nutrients · 2022Review
- Review
- The Cellular Senescence Stress Response in Post-Mitotic Brain Cells: Cell Survival at the Expense of Tissue Degeneration.Life (Basel, Switzerland) · 2021Review
- Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration.International journal of molecular sciences · 2020Review
- Intraperitoneal injection of IFN-γ restores microglial autophagy, promotes amyloid-β clearance and improves cognition in APP/PS1 mice.Cell death & disease · 2020Article
- Endothelial-specific deficiency of megalin in the brain protects mice against high-fat diet challenge.Journal of neuroinflammation · 2020Article
- Amarogentin fromOxidative medicine and cellular longevity · 2020Article
- Down Syndrome Is a Metabolic Disease: Altered Insulin Signaling Mediates Peripheral and Brain Dysfunctions.Frontiers in neuroscience · 2020Review
- Intergenerational Metabolic Syndrome and Neuronal Network Hyperexcitability in Autism.Trends in neurosciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
High sugar consumption and diabetes increase the risk of developing Alzheimer's disease (AD) by unknown mechanisms. Using an animal model of AD, here we show that high sucrose intake induces obesity with changes in central and peripheral insulin signaling. These pre-diabetic changes are associated with an increase in amyloid-β production and deposition. Moreover, high sucrose ingestion exacerbates tau phosphorylation by increasing Cdk5 activity. Mechanistically, the sucrose-mediated increase in AD-like pathology results from hyperactive mammalian target of rapamycin (mTOR), a key nutrient sensor important in regulating energy homeostasis. Specifically, we show that rapamycin, an mTOR inhibitor, prevents the detrimental effects of sucrose in the brain without altering changes in peripheral insulin resistance. Overall, our data suggest that high sucrose intake and dysregulated insulin signaling, which are known to contribute to the occurrence of diabetes, increase the risk of developing AD by upregulating brain mTOR signaling. Therefore, early interventions to modulate mTOR activity in individuals at high risk of developing diabetes may decrease their AD susceptibility.
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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.