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Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice
Open accessAbstract
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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“dietary restriction (i.e., the maintenance of a balanced diet) or addition of supplementary substances (e.g., omega-3 fatty acids; resveratrol) can induce an increase in BDNF levels and reduce cognitive impairment in animal models [224–226].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [225]
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Haritov, E., Garalova, M., Tivcheva, Y., Angelov, T., & Stamenov, V. (2020) · Acta Medica Bulgarica · doi:10.2478/amb-2020-0025 · Cited by 2
“Interestingly, dropping the number of calories consumed promotes the survival of newly created cells in the hippocampus [34].”
BackgroundHuntington's Disease and Other Choreas
Salman, H., Wild, E. J., & Tabrizi, S. J. (2017) · Neurodegeneration · doi:10.1002/9781118661895.ch21 · Cited by 2
The Involvement of Neuroimmune Cells in Adipose InnervationPreprint
Blaszkiewicz, M., Wood, E., Koizar, S., Willows, J. W., Anderson, R., Tseng, Y., Godwin, J. W., & Townsend, K. L. (2020) · Research Square · doi:10.21203/rs.3.rs-66882/v1 · Cited by 2
Molecular Pathogenesis and Therapeutic Targets in Huntington's Disease
Bett, J. S., Bates, G. P., & Hockly, E. (2006) · Elsevier eBooks · doi:10.1016/b978-012369462-1/50015-6 · Cited by 1
Poddar, M. K., & Chakraborty, A. (2019) · Acta Scientifci Nutritional Health · doi:10.31080/asnh.2019.03.0458
The Mediterranean style diet and cognition
Hardman, R. J., & Formica, M. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-818649-7.00039-4 · Cited by 1
Fasting and Caloric Restriction for Healthy Aging and Longevity
Sharma, S., & Kaur, G. (2021) · Healthy ageing and longevity · doi:10.1007/978-3-030-83017-5_24 · Cited by 1
Mitochondrial Dysfunction in Brain and Muscle Pathology of Huntington’s Disease
Rivera, S., McMurray, C. T., & Ayala‐Peña, S. (2014) · Springer eBooks · doi:10.1007/978-3-642-30018-9_133 · Cited by 1
Molecular and Biological Factors in Aging
Litke, R. R., & Mobbs, C. V. (2023) · Springer eBooks · doi:10.1007/978-3-030-01782-8_102-1 · Cited by 1
Role of protein-rich diet in brain functions
Ahire, E. D., Surana, K. R., Khairnar, S. J., Laddha, U. D., Kshirsagar, S. J., Rajora, A. K., & Keservani, R. K. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-18951-7.00026-8 · Cited by 1
Molecular and Biological Factors in Aging
Litke, R. R., & Mobbs, C. V. (2024) · Springer eBooks · doi:10.1007/978-3-030-74720-6_102 · Cited by 1
The search for energy: a driving force in evolution and aging
Mattson, M. P. (2003) · Advances in cell aging and gerontology · doi:10.1016/s1566-3124(03)14001-1 · Cited by 1
Self-citationDietary Modulation of Lipid Rafts
Mattson, M. P. (2005) · Humana Press eBooks · doi:10.1385/1-59259-803-x:191 · Cited by 1
“is enhanced by dietary restriction (Lee et al., 2002; Duan et al., 2003 ), and it has been shown that receptors for BDNF are located in lipid rafts (Higuchi et al., 2003).”
Self-citationOther Noteworthy Papers This Week
(2003) · Science of Aging Knowledge Environment · doi:10.1126/sageke.2003.7.nw28 · Cited by 1
Etiology, Pathology, and Pathogenesis
Weydt, P., Landwehrmeyer, G. B., & Ludolph, A. C. (2009) · Blue books of neurology · doi:10.1016/b978-1-4160-6641-5.00024-6
Sirtuins as Potential Drug Targets for Metabolic Diseases
Tong, Q. (2011) · Wiley eBooks · doi:10.1002/9780470910016.ch15
β-cell dysfunction in Huntington's disease
Bacos, K. (2009) · Lund University Publications (Lund University)
Burg, M., & Jorien, M. (2008) · Lund University Publications (Lund University)
Mehdipour, M., Zarifkar, A., & Namavar, M. R. (2015) · Journal of Advanced Medical Sciences and Applied Technologies · doi:10.18869/nrip.jamsat.1.1.42
Bouwknecht, J. A., & Enoch, M. (2004) · Genes Brain & Behavior · doi:10.1111/j.1601-1848.2004.00077.x
“Mattson’s work has shown that DR stimulates BDNF transcription in the hippocampus and pyramidal neurons, and BDNF signaling in the brain alters insulin sensitivity and regulates peripheral glucose metabolism (Duan et al. 2003).”
BackgroundMurine Models of Huntington Disease
Sturrock, A., & Leavitt, B. R. (2009) · Future Neurology · doi:10.2217/fnl.09.34
Study of novel pathogenic mechanisms in Huntington disease
Alberti, S. (2013)
Yanos, M. E. (2014) · ResearchWorks at the University of Washington (University of Washington)
Alteration of cholesterol homeostasis in the Huntington's disease brain
Kreilaus, F. (2015) · Research Online (University of Wollongong)
Gene–Environment Interactions in Huntington’s Disease
Bichell, T. J., Uhouse, M. A., Bradley, E. M., & Bowman, A. B. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-800228-5.00017-0
Metadata
- Authors
- Duan, W., Guo, Z., Jiang, H., Ware, M., Li, X.-J., & Mattson, M. P.
- Affiliations
- Johns Hopkins University (US)
- National Institutes of Health (US)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-02-14
- Volume
- 100
- Issue
- 5
- Pages
- 2911-2916
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC151440
- OpenAlex
- W1997887740
- Cited by
- 428
- References
- 59
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 14 · 2023: 8 · 2022: 17 · 2021: 13 · 2020: 18 · 2019: 19 · 2018: 18 · 2017: 22 · 2016: 13 · 2015: 18 · 2014: 26 · 2013: 18 · 2012: 16
- FWCI
- 10.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Keywords
- Huntington's disease, dietary restriction, brain-derived neurotrophic factor, HSP70, impaired glucose tolerance, hyperglycemia, tissue wasting, motor impairment, apoptosis, neurodegeneration, cellular stress resistance, lifespan extension, striatum, cortex
- MeSH terms
- Huntingtin Protein, Animals, Behavior, Animal, Blood Glucose, Brain, Cell Survival, Enzyme Activation, Enzyme-Linked Immunosorbent Assay, Glucose, Insulin, Male, Mice, Transgenic, Mutation, Nerve Tissue Proteins, Nuclear Proteins, Time Factors, Immunoblotting, Up-Regulation, Disease Progression, Brain-Derived Neurotrophic Factor, Neurodegenerative Diseases, Caspases, Leptin, Mice
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