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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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Self-citationModulating Neurotrophin Receptor Signaling as a Therapeutic Strategy for Huntington’s Disease
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“CR has long been recognized as a natural therapy that improves health and extends longevity in humans and rodents (Weindruch and Walford, 1988; Greene et al., 2001, 2003; Duan et al., 2003; Koubova and Guarente, 2003).”
BackgroundA critical review of brain and cognitive reserve in Huntington’s disease
Soloveva, M. V., Jamadar, S. D., Poudel, G. R., & Georgiou‐Karistianis, N. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.03.003 · Cited by 38
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“Perhaps voluntary exercise [27] or dietary restriction [28] in combination with high levels of cognitive and sensory stimulation is required to further delay the rotarod deficit in R6/1 mice.”
BackgroundRole of the hypothalamus in mediating protective effects of dietary restriction during aging
Dacks, P. A., Moreno, C. L., Kim, E. S., Marcellino, B. K., & Mobbs, C. V. (2012) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2012.12.001 · Cited by 38
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“& Modulation of AMPA-type glutamate receptor by ampakine CX929 [101, 102] & Modulation of signaling pathways, such as JNK and ERK (using CEP-1347), cAMP/CREB (using phosphodiesterase inhibitors rolipram and TP-10), or the Ask1 apoptotic pathway (using an anti-Ask1 antibody) [103–106] & Strategies aimed at reversing mi…”
MethodRatovitski, T., Chaerkady, R., Kammers, K., Stewart, J. C., Zavala, A., Pletniková, O., Troncoso, J. C., Rudnicki, D. D., Margolis, R. L., Cole, R. N., et al. (2016) · Journal of Proteome Research · doi:10.1021/acs.jproteome.6b00448 · Cited by 37
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“Restoring cortical BDNF levels in huntingtin mutant mice suppresses HD pathology and extends lifespan (Duan et al., 2003; Gharami et al., 2008).”
Self-citationLate-onset dementia: a mosaic of prototypical pathologies modifiable by diet and lifestyle
Mattson, M. P. (2015) · npj Aging and Mechanisms of Disease · doi:10.1038/npjamd.2015.3 · Cited by 34
Self-citationHigh stress hormone levels accelerate the onset of memory deficits in male Huntington's disease mice
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“It is also reported that mice with reduced BDNF levels become obese and exhibit insulin resistance and further intermittent fasting of these mice raised BDNF levels and improved glucose metabolism (Duan et al., 2003a,b).”
Mobbs, C. V., Mastaitis, J. W., Zhang, M., Isoda, F., Cheng, H., & Yen, K. (2006) · KARGER eBooks · doi:10.1159/000096555 · Cited by 35
“Furthermore, dietary restriction substantially ameliorates symptoms in a mouse transgenic model of Huntington's disease [136].”
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“It is also interesting that alternate day fasting for three months in HD transgenic mice reduced the amount of tissue wasting and weight loss when compared to mice eating ad libitum [85].”
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Self-citationSirtuin Deacetylases as Therapeutic Targets in the Nervous System
Langley, B. C., & Sauve, A. A. (2013) · Neurotherapeutics · doi:10.1007/s13311-013-0214-5 · Cited by 33
“Early studies in mutant HTT transgenic mice (N17182Q) showed that CR can delay the onset of motor dysfunction and prolong lifespan [157].”
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Diabetes and Stem Cell Function
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“Diabetes frequently develops in HD patients [82] and in transgenic mouse models of HD such as the R6/2, HD-N171-82Q mice [83, 84].”
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BackgroundIntermittent fasting and neurodegenerative diseases: Molecular mechanisms and therapeutic potential
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“This approach has proven effective in mouse models of PD (Duan et al., 1999) and HD (Duan et al., 2003).”
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“Some treatments like caloric restriction (Duan et al., 2003) or environmental enrichment (Spires et al., 2004) that have been shown to slow down the course of the disease in transgenic mice have also been reported to increase BDNF levels in some areas of the brain.”
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“Neuroprotection may be mediated by increased production of brain-derived neurotrophic factor (Duan et al., 2001a; Duan et al., 2001b ) and protein chaperones (Lee et al., 1999; Guo et al., 2000).”
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“In addition, increased glucose plasma levels have also been observed in different models expressing HTT with shorter polyQ repeats (82Q and 89Q) [117, 118].”
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“Caloric restriction (CR), the reduction of nutrient intake without malnutrition, is a natural therapy that improves health and extends longevity (Weindruch and Walford 1988; Greene et al. 2001; Duan et al. 2003; Denny et al. 2006).”
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“, via intermittent fasting or periodically reduced food intake (Duan et al., 2003; Gregosa et al., 2019; Moreno et al., 2016).”
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“reported that dietary restriction increased levels of brain-derived neurotrophic factor and heatshock protein-70 in the striatum and cortex, retarded the formation of Htt inclusions, apoptotic protease activation, enhanced movement in HD mice and extended lifespan [78].”
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“Activation of this pathway by BDNF has a crucial role in learning and memory, is neuroprotective in models of Alzheimer, Parkinson and Huntington diseases, and improves peripheral glucose metabolism by enhancing insulin sensitivit”
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“A later motor phenotype is common for N17182Q mice, while tremors, gait disturbances, and altered rotarod performance occur between 2 to 3 months of age (Chiu, Liu, Leeds, & Chuang, 2011; Duan et al., 2003; Masuda et al., 2008; Schilling et al., 1999, 2004).”
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“…diseases like Alzheimer’s disease (Mattson 2000a, b, 2003a, b; Patel et al. 2005; Wang et al. 2005; Zhu et al. 1999), Huntington’s disease (Duan et al. 2003), Amyotrophic Lateral Sclerosis (Hamadeh et al. 2005) and PD (Table 1) (Duan and Mattson 1999; Holmer et al. 2005; Mattson 2003a,…”
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“Calorie restriction and intermittent fasting delay structural and functional age-related decline in rodents and monkeys (Duan et al., 2003; Willette et al., 2010; Mattison et al., 2012).”
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Targeting energy metabolism in Huntington's disease
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The role of cannabinoids and leptin in neurological diseases
Agar, E. (2015) · Acta Neurologica Scandinavica · doi:10.1111/ane.12411 · Cited by 21
“Leptin levels were slightly higher in a dietary restricted mouse model of HD in animals with decreased weight loss (76).”
BackgroundNo evidence of association between BDNF gene variants and age-at-onset of Huntington's disease
Maria, E. D., Marasco, A., Tartari, M., Ciotti, P., Abbruzzese, G., Novelli, G., Bellone, E., Cattaneo, E. F., & Mandich, P. (2006) · Neurobiology of Disease · doi:10.1016/j.nbd.2006.07.002 · Cited by 20
The Heat Shock Connection of Metabolic Stress and Dietary Restriction
Dancsó, B., Spiró, Z., Arslan, M. A., Nguyen, M., Papp, D., Csermely, P., & Sőti, C. (2010) · Current Pharmaceutical Biotechnology · doi:10.2174/138920110790909704 · Cited by 20
Calcium-dependent and aspartyl proteases in neurodegeneration and ageing in C. elegans
Samara, C., & Tavernarakis, N. (2003) · Ageing Research Reviews · doi:10.1016/s1568-1637(03)00032-1 · Cited by 19
Metabolic Alterations at the Crossroad of Aging and Oncogenesis
Raffaghello, L., & Longo, V. D. (2017) · International review of cytology · doi:10.1016/bs.ircmb.2017.01.003 · Cited by 19
“…disease (Halagappa et al., 2007), reduces degeneration of dopaminergic neurons in models of Parkinson’s disease (Duan and Mattson, 1999), and slows disease progression in huntingtin mutant mice by normalizing glucose metabolism and brain-derived neurotrophic factor levels (Duan et al., 2003).”
Backgroundda Fonsêca, V. S., Colla, A. R. D. S., Nascimento-Castro, C. D. P., Plácido, E., Rosa, J. M., Farina, M., Gil‐Mohapel, J., Rodrigues, A. L. S., & Brocardo, P. S. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-0890-6 · Cited by 19
“Indeed, pharmacological and non-pharmacological strategies that are thought to result in increased BDNF levels, such as dietary restriction [108], physical exercise [109], environmental enrichment [110], immunomodulator drugs [111], and/ or antidepressant (i.”
BackgroundNemo-like kinase reduces mutant huntingtin levels and mitigates Huntington’s disease
Jiang, M., Zhang, X., Liu, H., LeBron, J., Alexandris, A., Peng, Q., Gu, H., Yang, F., Li, Y., Wang, R., et al. (2020) · Human Molecular Genetics · doi:10.1093/hmg/ddaa061 · Cited by 15
“Male N171-82Q mice were used in our studies because of gender-dependent phenotypic differences in these HD mice (56).”
MethodSelf-citationCorey‐Bloom, J., Aikin, A. M., Gutierrez, A. M., Nadhem, J. S., Howell, T. L., & Thomas, E. A. (2017) · Brain Research · doi:10.1016/j.brainres.2017.08.013 · Cited by 17
“2001) and in several different mouse models transgenic for mutant huntingtin, including R6/2, YAC72 and N171-82Q transgenic mice (Duan et al. 2003; Zhang et al. 2003; Zuccato et al. 2001).”
BackgroundOsteocalcin and GPR158: linking bone and brain function
Li, J., Lou, S., & Bian, X. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2025.1564751 · Cited by 20
Jambi, E. J., Alamri, A. M., Afzal, M., Al-Abbasi, F. A., Al-Qahtani, S. D., Almalki, N. A. R., Bawadood, A. S., Alzarea, S. I., Sayyed, N., & Kazmi, I. A. (2024) · PLoS ONE · doi:10.1371/journal.pone.0305358 · Cited by 16
Dietary restriction and brain health
Qiu, G., Liu, S., & So, K. (2010) · Neuroscience Bulletin · doi:10.1007/s12264-010-0716-7 · Cited by 18
Dietary Restriction and Glycolytic Inhibition Reduce Proteotoxicity and Extend Lifespan via NHR-49.
Marcellino, B. K., Ekasumara, N., & Mobbs, C. V. (2018) · PubMed · Cited by 16
Development of novel therapies for Huntington's disease: hope and challenge1
Qin, Z., Wang, J., & Gu, Z. (2005) · Acta Pharmacologica Sinica · doi:10.1111/j.1745-7254.2005.00520.x · Cited by 16
Effect of Body Weight on Age at Onset in Huntington Disease
van der Burg, J. M. M., Weydt, P., Landwehrmeyer, G. B., & Aziz, N. A. (2021) · Neurology Genetics · doi:10.1212/nxg.0000000000000603 · Cited by 15
Dkhar, P., & Sharma, R. (2013) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-013-0015-8 · Cited by 15
Could metformin be therapeutically useful in Huntington’s disease?
Tang, B. L. (2019) · Reviews in the Neurosciences · doi:10.1515/revneuro-2019-0072 · Cited by 15
Disease Modifying Potential of Glatiramer Acetate in Huntington's Disease
Corey‐Bloom, J., Jia, H., Aikin, A. M., & Thomas, E. A. (2014) · Journal of Huntington s Disease · doi:10.3233/jhd-140110 · Cited by 15
“Accordingly, BDNF is decreased in brain tissue from human HD patients [13, 17] and in HD transgenic mice [13, 18, 19].”
Effects of lifespan-extending interventions on cognitive healthspan
Čulig, L., Sahbaz, B. D., & Bohr, V. A. (2022) · Expert Reviews in Molecular Medicine · doi:10.1017/erm.2022.36 · Cited by 14
Recommendations for the Treatment of Patients With Parkinson Disease During Ramadan
Damier, P., & Al-Hashel, J. Y. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2016.4291 · Cited by 14
Molecular connections of obesity and aging: a focus on adipose protein 53 and retinoblastoma protein
Chu, D., & Tao, Y. (2017) · Biogerontology · doi:10.1007/s10522-017-9698-4 · Cited by 14
Bandô, Y., & Geisler, J. G. (2019) · Neurochemistry International · doi:10.1016/j.neuint.2019.104561 · Cited by 14
Tallaksen‐Greene, S. J., Sadagurski, M., Zeng, L., Mauch, R. J., Perkins, M., Banduseela, V. C., Lieberman, A. P., Miller, R. A., Paulson, H. L., & Albin, R. L. (2014) · Journal of Neuroscience · doi:10.1523/jneurosci.1830-14.2014 · Cited by 14
“Caloric restriction, for example, is reported to have beneficial effects in a C. elegans polyQ disease model and the R6/2 model of HD (Duan et al., 2003).”
BackgroundThree Effective Ways to Nurture Our Brain
Misuraca, R., Miceli, S., & Teuscher, U. (2017) · European Psychologist · doi:10.1027/1016-9040/a000284 · Cited by 17
“Caloric restriction has also been found to be associated with high levels of BDNF (Duan et al., 2003; Lee, Seroogy, & Mattson, 2002), which, as previously mentioned, is a key factor for the promotion of synaptic plasticity.”
BackgroundMattson, M. P. (2017) · Neurodegeneration · doi:10.1002/9781118661895.ch4 · Cited by 17
Self-citationMolinaro, G., Battaglia, G., Riozzi, B., Storto, M., Fucile, S., Eusebi, F., Nicoletti, F., & Bruno, V. (2007) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2007.10.009 · Cited by 13
Mechanistic target of rapamycin signaling in mouse models of accelerated aging
Lee, J. Y., Kennedy, B. K., & Liao, C. (2019) · The Journals of Gerontology Series A · doi:10.1093/gerona/glz059 · Cited by 13
“In the same mouse model; however, DR slows down the disease progression and extends life span (38).”
Grados, M. A., Sung, H. M., Kim, S.-J., & Srivastava, S. (2014) · Drug Development Research · doi:10.1002/ddr.21223 · Cited by 11
“, 2008] or dietary restriction in a mouse model of Huntington disease [Duan et al., 2003] have similar results.”
ResultRoss, C. A., Kronenbuerger, M., Duan, W., & Margolis, R. L. (2017) · Handbook of clinical neurology · doi:10.1016/b978-0-12-801893-4.00002-x · Cited by 14
Self-citationNeural network plasticity, BDNF and behavioral interventions in Alzheimer's disease
Hubka, P. (2006) · Bratislavské lekárske listy/Bratislava medical journal · doi:10.1007/bf03656858 · Cited by 12
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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