ArticleProceedings of the National Academy of Sciences of the United States of America2003
Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 papers.
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Who cites it
202 citing papers in PubMed, 423 citations in OpenAlex.
- Effects of time-restricted eating in early-stage Huntington's disease: a pilot study.Nature metabolism · 2026Trial
- Intranasal insulin for improving cognitive function in multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Trial
- Meal timing as medicine: clinical evidence for intermittent fasting in Huntington's disease.Nature metabolism · 2026Article
- Profiles of patients at early stages of Huntington's disease based on the routine biological markers and the disease progression.Journal of neurology · 2026Article
- Dietary restriction as a potential neuroprotective intervention: a narrative review of its impact on neuroinflammation across neurodegenerative diseases and other neurological disorders.Frontiers in nutrition · 2026Review
- Glucose restriction induces degeneration of neurons with mitochondrial DNA depletion by altering ER-mitochondria calcium transfer.Molecular psychiatry · 2025Article
- Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson's disease.Nature communications · 2025Article
- Time-restricted eating in early-stage Huntington's disease: A 12-week interventional clinical trial protocol.PloS one · 2025Article
- Osteocalcin and GPR158: linking bone and brain function.Frontiers in cell and developmental biology · 2025Review
- Neuroprotective effects of levothyroxine on cognition deficits and memory in an experimental model of Huntington's disease in rats: An electrophysiological study.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Brain-Periphery Interactions in Huntington's Disease: Mediators and Lifestyle Interventions.International journal of molecular sciences · 2024Review
- Dietary fasting and time-restricted eating in Huntington's disease: therapeutic potential and underlying mechanisms.Translational neurodegeneration · 2024Review
- Effects of dietary intervention on human diseases: molecular mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2024Review
- Article
- Intermittent fasting, fatty acid metabolism reprogramming, and neuroimmuno microenvironment: mechanisms and application prospects.Frontiers in nutrition · 2024Review
- BDNF and Cerebellar Ataxia.Current drug research reviews · 2024Review
- GPR37 and its neuroprotective mechanisms: bridging osteocalcin signaling and brain function.Frontiers in cell and developmental biology · 2024Review
- Fasting: From Physiology to Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Review
- Diapocynin neuroprotective effects in 3-nitropropionic acid Huntington's disease model in rats: emphasis on Sirt1/Nrf2 signaling pathway.Inflammopharmacology · 2022Article
142 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
In addition to neurological deficits, Huntington's disease (HD) patients and transgenic mice expressing mutant human huntingtin exhibit reduced levels of brain-derived neurotrophic factor, hyperglycemia, and tissue wasting. We show that the progression of neuropathological (formation of huntingtin inclusions and apoptotic protease activation), behavioral (motor dysfunction), and metabolic (glucose intolerance and tissue wasting) abnormalities in huntingtin mutant mice, an animal model of HD, are retarded when the mice are maintained on a dietary restriction (DR) feeding regimen resulting in an extension of their life span. DR increases levels of brain-derived neurotrophic factor and the protein chaperone heat-shock protein-70 in the striatum and cortex, which are depleted in HD mice fed a normal diet. The suppression of the pathogenic processes by DR in HD mice suggests that mutant huntingtin promotes neuronal degeneration by impairing cellular stress resistance, and that the body wasting in HD is driven by the neurodegenerative process. Our findings suggest a dietary intervention that may suppress the disease process and increase the life span of humans that carry the mutant huntingtin gene.
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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.