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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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“Indeed, increasing striatal BDNF levels via pharmacological or behavioral stimulation that induces Bdnf gene expression (Duan et al., 2003; Spires et al., 2004; Peng et al., 2008; Simmons et al., 2009) or by viral delivery (Cho et al., 2007), improves disease phenotypes in several HD mouse models.”
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“Intrigueingly, a dietary restriction regimen that has been shown to increase BDNF levels in the cerebral cortex, striatum, and hippocampus of mice and rats, was found to increase survival, improve motor performance, ameliorate weight loss, and delay huntingtin aggegate formation and systemic glucose intolerance in R6/…”
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“In line with this notion, several genetic, pharmacological, and dietary anti-aging interventions have been reported to ameliorate aspects of HD in mouse models (Duan et al., 2003; Ma et al., 2007; Sadagurski et al., 2011; Tallaksen-Greene et al., 2014; Moreno et al., 2016).”
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“Interestingly, dietary restriction — the only manipulation that consistently increases the lifespan of mammals — improves survival of these mice by about two week”
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“SIRT1 protects against some models of neurodegeneration, although unlike CR, which convincingly delays neurodegeneration (Bruce-Keller et al., 1999; Duan et al., 2003; Maswood et al., 2004), the protective role of SIRT1 remains controversial.”
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“344 A cross-sectional baseline analysis revealed that a higher intake of antioxidants and carotenes may result in greater ALS function.”
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“BDNF levels significantly increase in mice on regimens of dietary restriction (14) or physical exercise favored by environmental enrichment (46).”
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Self-citationNew Avenues for the Treatment of Huntington’s Disease
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“Although it is possible to increase BDNF levels with dietary interventions [109,273] or through environmental enrichment [274,275] and physical activity [113,276,277], here, we focus on the direct up-regulation of this neurotrophin through protein infusion, genetic approaches, and pharmacological strategies.”
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Self-citationAxonal Degeneration during Aging and Its Functional Role in Neurodegenerative Disorders
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“Importantly, studies aimed at determine the effect of caloric restriction in NDs have shown positive outcomes using models of AD (Wu et al., 2008), PD (Maswood et al., 2004), andHuntington disease (HD; Duan et al., 2003).”
BackgroundMolecular and cellular pathways contributing to brain aging
Zia, A., Pourbagher‐Shahri, A. M., Farkhondeh, T., & Samarghandian, S. (2021) · Behavioral and Brain Functions · doi:10.1186/s12993-021-00179-9 · Cited by 195
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“Furthermore, CR stimulates the secretion of neurotrophic factors and relieves diverse stress responses as well as DNA maintenance in mice.(289,290) Added to the diet cycle and components, FMD contributes to improved cognitive performance in aged mice and in humans through elevation of NeuroD1 but reduced IGF-1 levels…”
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Self-citationIntermittent Food Deprivation Improves Cardiovascular and Neuroendocrine Responses to Stress in Rats
Wan, R., Camandola, S., & Mattson, M. P. (2003) · Journal of Nutrition · doi:10.1093/jn/133.6.1921 · Cited by 175
“For example, both IF and energy restriction decrease blood glucose and insulin levels, and increase corticosterone levels (7,34,35).”
BackgroundSelf-citationCGS21680 attenuates symptoms of Huntington's disease in a transgenic mouse model
Chou, S., Lee, Y., Chen, H., Chiang, M., Lai, H., Chang, H., Wu, Y., Sun, C., Chien, C., Lin, Y., et al. (2005) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2005.03029.x · Cited by 179
“…in both HD patients and in R6/2 mice (Podolsky et al. 1972), and because suppressed hyperglycemia has been associated with improvement in neurological deficits of HD (Duan et al. 2003), we performed experiments to determine whether chronic CGS treatment normalized the usage of glucose in R6/2 mice.”
BackgroundMethodInfluentialPeng, Q., Masuda, N., Jiang, M., Li, Q., Zhao, M., Ross, C. A., & Duan, W. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2007.10.015 · Cited by 177
“BDNF protein levels were quantified by BDNF Emax Immunoassay (Promega) as described previously (Duan et al., 2003).”
BackgroundMethodInfluentialSelf-citationNELSON, R., GUO, Z., HALAGAPPA, V, PEARSON, M., GRAY, A., MATSUOKA, Y., BROWN, M., MARTIN, B., IYUN, T., & MAUDSLEY, S. (2007) · Experimental Neurology · doi:10.1016/j.expneurol.2007.01.037 · Cited by 173
Self-citationRecruiting adaptive cellular stress responses for successful brain ageing
Stranahan, A. M., & Mattson, M. P. (2012) · Nature reviews. Neuroscience · doi:10.1038/nrn3151 · Cited by 170
“models of Parkinson's disease, protecting striatal and cortical neurons, and extending survival in a mouse model of Huntington's diseas”
BackgroundSelf-citationDey, N. D., Bombard, M. C., Roland, B. P., Davidson, S., Lü, M., Rossignol, J., Sandstrom, M. I., Skeel, R. L., Lescaudron, L., & Dunbar, G. L. (2010) · Behavioural Brain Research · doi:10.1016/j.bbr.2010.05.023 · Cited by 169
Yao, J., Chen, S., Mao, Z., Cadenas, E., & Brinton, R. D. (2011) · PLoS ONE · doi:10.1371/journal.pone.0021788 · Cited by 169
“Further, caloric restriction has been demonstrated to up-regulate expression of neurotrophic factors such as BDNF [46,47,48], which was also achieved by dietary 2DG administration in the current study.”
BackgroundInfluentialGreene, A. E., Todorova, M. T., & Seyfried, T. N. (2003) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2003.01862.x · Cited by 166
“Caloric restriction (CR) is a natural dietary therapy that improves health, extends longevity and reduces the effects of neuroinflammatory diseases in rodents and humans (Weindruch and Walford 1988; Mattson et al. 2001; Mukherjee et al. 2002; Duan et al. 2003; Koubova and Guarente 2003).”
BackgroundMattson, M. P. (2004) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1306.004 · Cited by 162
Self-citationGene expression in Huntington's disease skeletal muscle: a potential biomarker
Strand, A. D., Aragaki, A. K., Shaw, D., Bird, T. D., Holton, J. L., Turner, C., Tapscott, S. J., Tabrizi, S. J., Schapira, A. H. V., Kooperberg, C. L., et al. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi192 · Cited by 160
Moffitt, H., McPhail, G., Woodman, B., Hobbs, C., & Bates, G. P. (2009) · PLoS ONE · doi:10.1371/journal.pone.0008025 · Cited by 151
“As mentioned above, PGC-1a activity is also decreased in muscle from HD patients and N171-82Q mice [35] and given the pathology that we have described in R6/2 and HdhQ150/Q150 liver, an investigation of the UCPs in liver is warranted.”
BackgroundInfluentialAssessment of the nutrition status of patients with Huntington's disease
Contreras, A. T., Tarrats, R. M., Alonso, M. E., Boll, M., Ochoa, A., & Velásquez, L. (2004) · Nutrition · doi:10.1016/j.nut.2003.10.007 · Cited by 156
Masino, S. A., Kawamura, M., Wasser, C. R., Pomeroy, L. S., & Ruskin, D. N. (2009) · Current Neuropharmacology · doi:10.2174/157015909789152164 · Cited by 155
“As one example, metabolic therapy may offer symptomatic delay or improvement even in a genetic, neurodegenerative disorder such as Huntington’s disease [41, 186].”
BackgroundLifelong brain health is a lifelong challenge: From evolutionary principles to empirical evidence
Mattson, M. P. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2014.12.011 · Cited by 161
Self-citationSynaptic plasticity in the ischaemic brain
Calabresi, P., Centonze, D., Pisani, A., Cupini, L. M., & Bernardi, G. (2003) · The Lancet Neurology · doi:10.1016/s1474-4422(03)00532-5 · Cited by 154
Leptin neuroprotection in the CNS: mechanisms and therapeutic potentials
Signore, A. P., Zhang, F., Weng, Z., Gao, Y., & Chen, J. (2008) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2008.05457.x · Cited by 157
Glucose Homeostasis in Huntington Disease
Lalic, N. M., Marić, J., Svetel, M. V., Jotić, A., Stefanova, E. D., Lalic, K. S., Dragašević, N., Milicic, T. J., Lukić, L., & Kostić, V. (2008) · Archives of Neurology · doi:10.1001/archneur.65.4.476 · Cited by 150
“The same effect on brain-derived growth factor was also found with food restriction, which paradoxically slowed disease progression and weight loss in HD transgenic mice.(30) Yamamoto et al(32) demonstrated that activation of insulin receptor substrate 2, a scaffolding protein that mediates the signaling cascades of g…”
The influences of diet and exercise on mental health through hormesis
Gómez‐Pinilla, F. (2007) · Ageing Research Reviews · doi:10.1016/j.arr.2007.04.003 · Cited by 158
“It is also known that CR elevates levels of BDNF (Lee et al., 2002; Duan et al., 2003), and that BDNF may mediate the effect of CR on increasing hippocampal neurogenesis (Lee et al.”
BackgroundResveratrol protects against peripheral deficits in a mouse model of Huntington's disease
Ho, D. J., Calingasan, N. Y., Wille, E. J., Dumont, M., & Beal, M. F. (2010) · Experimental Neurology · doi:10.1016/j.expneurol.2010.05.006 · Cited by 148
Chronic Intermittent Fasting Improves Cognitive Functions and Brain Structures in Mice
Li, L., Wang, Z., & Zuo, Z. (2013) · PLoS ONE · doi:10.1371/journal.pone.0066069 · Cited by 147
“in the brain of Huntingtin mutant mice after caloric restriction [14].”
BackgroundExercise, Energy Intake, Glucose Homeostasis, and the Brain
van Praag, H., Fleshner, M., Schwartz, M. W., & Mattson, M. P. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.2814-14.2014 · Cited by 157
“, 2007), Huntington’s (Duan et al., 2003), and Charcot-Marie-Tooth (Madorsky et al.”
BackgroundInfluentialSelf-citationSimmons, D. A., Belichenko, N. P., Yang, T., Condon, C., Monbureau, M., Shamloo, M., Jing, D., Massa, S. M., & Longo, F. M. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.1310-13.2013 · Cited by 145
“…are reduced in HD patients (Ferrer et al., 2000; Gauthier et al., 2004) and numerous HD mouse models (Zuccato et al., 2001; Luthi-Carter et al., 2002; Duan et al., 2003; Gines et al., 2003; Spires et al., 2004a; Lynch et al., 2007; Simmons et al., 2009), including R6/2 mice (Simmons et al., 2011).”
BackgroundInfluentialFasting Therapy for Treating and Preventing Disease - Current State of Evidence
Michalsen, A., & Li, C. (2013) · Complementary Medicine Research · doi:10.1159/000357765 · Cited by 146
Duan, W., Peng, Q., Masuda, N., Ford, E., Tryggestad, E. J., Ladenheim, B., Zhao, M., Cadet, J. L., Wong, J., & Ross, C. A. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.01.015 · Cited by 143
“BDNF protein levels were quantified by the BDNF Emax Immunoassay (Promega) as described previously (Duan et al., 2003).”
BackgroundMethodInfluentialSelf-citationChiu, C., Liu, G., Leeds, P. R., & Chuang, D. (2011) · Neuropsychopharmacology · doi:10.1038/npp.2011.128 · Cited by 146
“Decreased BDNF has been reported in the striatum of human HD patients (Ferrer et al, 2000; Zuccato et al, 2001) as well as in animal models of HD (Duan et al, 2003, 2008).”
Björkqvist, M., Fex, M., Renström, E., Wierup, N., Petersén, Å., Gil‐Mohapel, J., Bacos, K., Popović, N., Li, J., Sundler, F., et al. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi053 · Cited by 143
“Hyperglycemia has also been observed in the HD-N171-82Q mouse (39).”
BackgroundChronic Inflammation in the Context of Everyday Life: Dietary Changes as Mitigating Factors
Margina, D. M., Ungurianu, A., Purdel, C. N., Tsoukalas, D., Sarandi, E., Thanasoula, M., Tekos, F., Mesnage, R., Kouretas, D., & Tsatsakis, A. M. (2020) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph17114135 · Cited by 146
Role of molecular chaperones in neurodegenerative disorders
Meriin, A. B., & Sherman, M. Y. (2005) · International Journal of Hyperthermia · doi:10.1080/02656730500041871 · Cited by 135
“Furthermore, the delay in ageing in mice caused by a caloric restriction, a treatment, known to expand the animal’s lifespan, led to a significant reduction in polyQ aggregation, reduced brain atrophy and a delay in development of behavioural symptoms of the disease [128].”
BackgroundCommunication breakdown: The impact of ageing on synapse structure
Petralia, R. S., Mattson, M. P., & Yao, P. J. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.01.003 · Cited by 138
Self-citationHormesis/preconditioning mechanisms, the nervous system and aging
Arumugam, T. V., Gleichmann, M., Tang, S., & Mattson, M. P. (2006) · Ageing Research Reviews · doi:10.1016/j.arr.2006.03.003 · Cited by 131
Self-citationJiang, M., Peng, Q., Liu, X., Jin, J., Hou, Z., Zhang, J., Mori, S., Ross, C. A., Ye, K., & Duan, W. (2013) · Human Molecular Genetics · doi:10.1093/hmg/ddt098 · Cited by 131
“Male mice were used in our studies because we found gender-dependent phenotypic differences in N171-82Q HD mice (13).”
MethodSelf-citation
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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