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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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Cites
Adams, J., Dinesh, K., Xiong, M., Tarolli, C. G., Sharma, S., Sheth, N., Aranyosi, A. J., Zhu, W. Y., Goldenthal, S. B., Biglan, K., et al. (2017) · Digital Biomarkers · doi:10.1159/000479018 · Cited by 3,190
Davies, S. W., Turmaine, M., Cozens, B. A., DiFiglia, M., Sharp, A. H., Ross, C. A., Scherzinger, E., Wanker, E. E., Mangiarini, L., & Bates, G. P. (1997) · Cell · doi:10.1016/s0092-8674(00)80513-9 · Cited by 2,188
Replication of the neurochemical characteristics of Huntington's disease by quinolinic acid
Beal, M. F., Kowall, N. W., Ellison, D. W., Mazurek, M. F., Swartz, K. J., & Martin, J. B. (1986) · Nature · doi:10.1038/321168a0 · Cited by 1,287
Andrew, S. E., Goldberg, Y. P., Kremer, B. P. H., Telenius, H., Theilmann, J., Adam, S., Starr, E. M., Squitieri, F., Lin, B., Kalchman, M. A., et al. (1993) · Nature Genetics · doi:10.1038/ng0893-398 · Cited by 1,135
Loss of Huntingtin-Mediated BDNF Gene Transcription in Huntington's Disease
Zuccato, C., Ciammola, A., Rigamonti, D., Leavitt, B. R., Goffredo, D., Conti, L., MacDonald, M. E., Friedlander, R. M., Silani, V., Hayden, M. R., et al. (2001) · Science · doi:10.1126/science.1059581 · Cited by 1,123
Lee, J., Duan, W., & Mattson, M. P. (2002) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.2002.01085.x · Cited by 975
Self-citationDifferential loss of striatal projection neurons in Huntington disease.
Reiner, A., Albin, R. L., Anderson, K. D., D'Amato, C. J., Penney, J. B., & Young, A. B. (1988) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.85.15.5733 · Cited by 839
BDNF regulates eating behavior and locomotor activity in mice
Kernie, S. G., Liebl, D. J., & Parada, L. F. (2000) · The EMBO Journal · doi:10.1093/emboj/19.6.1290 · Cited by 806
Rios, M., Fan, G., Fekete, C., Kelly, J., Bates, B., Kuehn, R., Lechan, R. M., & Jaenisch, R. (2001) · Molecular Endocrinology · doi:10.1210/mend.15.10.0706 · Cited by 781
Schilling, G. (1999) · Human Molecular Genetics · doi:10.1093/hmg/8.3.397 · Cited by 772
Flagged first, then by citations
Research works printed but not linked: 2
- S E Andrew, Y P Goldberg, B Kremer, H Telenius, J Theilmann, S Adam, E Starr, F Squitieri, B Lin, M A Kalchman, et al. Nat Genet 7, 513–519 (1993).
- A R Heydari, C C Conrad, A Richardson J Nutr 125, 410–418 (1995).
Cited by
Sorted by citations
Items 101–200 of 426
Marini, A. M., Jiang, X., Wu, X., Tian, F., Zhu, D., Okagaki, P., & Lipsky, R. H. (2004) · PubMed · Cited by 128
Mattson, M. P., Duan, W., Wan, R., & Guo, Z. (2004) · Neurotherapeutics · doi:10.1602/neurorx.1.1.111 · Cited by 133
“The degeneration of striatal neurons was attenuated, the onset of motor dysfunction was delayed, and lifespan was increased in huntingtin mutant mice when they were maintained on a DR diet.(16) Finally, the ability of DR to improve outcome after a stroke was demonstrated in a rat model in which the middle cerebral art…”
BackgroundSelf-citationYoung, J. E., Martinez, R. A., & Spada, A. R. L. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m806088200 · Cited by 132
Mouse models of ageing and their relevance to disease
Kõks, S., Dogan, S., Tuna, B. G., González-Navarro, H., Potter, P., & Vandenbroucke, R. E. (2016) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2016.10.001 · Cited by 125
“…diseases such as Alzheimer’s, Parkinson’s and Huntington’s diseases and stroke (Van Cauwenberghe et al., 2016; Bondolfi et al., 2004; Patel et al., 2005; Wang et al., 2005; Park et al., 2013; Wu et al., 2008; Halagappa et al., 2007; Hornsby et al., 2016; Duan et al., 2003; Mattson et al., 2003).”
BackgroundNumakawa, T., Matsumoto, T., Numakawa, Y., Richards, M., Yamawaki, S., & Kunugi, H. (2011) · Journal of Toxicology · doi:10.1155/2011/405194 · Cited by 125
“Woronowicz et al. showed that TS induced phosphorylation of TrkB in rat pheochromocytoma (PC12) cells expressing TrkB and promoted cell survival under H2O2 stress [75].”
BackgroundCaloric restriction: Beneficial effects on brain aging and Alzheimer’s disease
Van Cauwenberghe, C., Vandendriessche, C., Libert, C., & Vandenbroucke, R. E. (2016) · Mammalian Genome · doi:10.1007/s00335-016-9647-6 · Cited by 121
“…mutant mice model (N171-82 Q), the formation of huntingtin inclusions and apoptotic protease activation, motor dysfunction, and metabolic glucose intolerance were delayed by a dietary restriction regime, which also slows down the disease progression and extended their lifespan (Duan et al. 2003).”
BackgroundIncreased peripheral lipid clearance in an animal model of amyotrophic lateral sclerosis
Fergani, A., Oudart, H., de Aguilar, J. G., Fricker, B., René, F., Hocquette, J.-F. J.-F., Meininger, V., Dupuis, L., & Loeffler, J. (2007) · Journal of Lipid Research · doi:10.1194/jlr.m700017-jlr200 · Cited by 131
“Contrary to animal models of Parkinson’s disease (38) and Huntington’s disease (39), in which caloric restriction has been shown to alleviate symptoms, caloric restriction shortens disease duration in mSOD1 mice (21).”
ResultJin, J., Albertz, J., Guo, Z., Peng, Q., Rudow, G. L., Troncoso, J. C., Ross, C. A., & Duan, W. (2013) · Journal of Neurochemistry · doi:10.1111/jnc.12190 · Cited by 120
“BDNF deficiency occurs commonly in HD patients as well as in HD mouse models, including N171-82Q HD mice (Duan et al. 2003).”
BackgroundMethodInfluentialSelf-citationThe metabolic profile of early Huntington's disease- a combined human and transgenic mouse study
Goodman, A. O. G., Murgatroyd, P. R., Medina‐Gómez, G., Wood, N. I., Finer, N., Vidal‐Puig, A., Morton, A. J., & Barker, R. A. (2008) · Experimental Neurology · doi:10.1016/j.expneurol.2007.12.026 · Cited by 118
“Stratified muscle wasting in transgenic mice has been shown previously (Duan et al., 2003; Sathasivam et al., 1999; LuthiCarter et al., 2002; Ribchester et al., 2004).”
BackgroundDietary restriction started after spinal cord injury improves functional recovery
Plunet, W. T., Streijger, F., Lam, C. K., Lee, J. H. T., Liu, J., & Tetzlaff, W. (2008) · Experimental Neurology · doi:10.1016/j.expneurol.2008.04.011 · Cited by 117
“DR can also have a direct effect on the cell death pathways by increasing anti-apoptotic proteins (ARC), along with decreasing pro-apoptotic proteins (caspase-1, caspase-2 activation, and cytochrome c release) (Duan et al., 2003; Shelke and Leeuwenburgh, 2003).”
BackgroundWu, P., Shen, Q., Dong, S., Xu, Z., Tsien, J. Z., & Hu, Y. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2007.03.028 · Cited by 118
Energy Intake and Amyotrophic Lateral Sclerosis
Mattson, M. P., Cutler, R. G., & Camandola, S. (2006) · NeuroMolecular Medicine · doi:10.1385/nmm:9:1:17 · Cited by 115
“For example, energy restriction suppressed the disease process and improved functional outcome in animal models of Parkinson’s (Maswood et al., 2004), Alzheimer’s (Patel et al., 2005), and Huntington’s ( Duan et al., 2003 ) diseases, and stroke (Yu and Mattson, 1999).”
BackgroundSelf-citationPerspective: Does brown fat protect against diseases of aging?
Mattson, M. P. (2009) · Ageing Research Reviews · doi:10.1016/j.arr.2009.11.004 · Cited by 114
Self-citationCunha-Santos, J., Duarte-Neves, J., Carmona, V., Guarente, L., Pereira de Almeida, L., & Cavadas, C. (2016) · Nature Communications · doi:10.1038/ncomms11445 · Cited by 109
Neuronutrition and Alzheimer's Disease
Ramesh, B. N., Rao, T. S., Prakasam, A., Sambamurti, K., & Rao, K. S. J. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-1312 · Cited by 113
“Rats maintained on CR show increased levels of BDNF in neurons in cerebral cortex, hippocampus, and striatum [48,49].”
Mantis, J. G., Centeno, N. A., Todorova, M. T., McGowan, R., & Seyfried, T. N. (2004) · Nutrition & Metabolism · doi:10.1186/1743-7075-1-11 · Cited by 108
A retrospective study of the impact of lifestyle on age at onset of Huntington disease
Trembath, M. K., Horton, Z., Tippett, L. J., Hogg, V. M., Collins, V., Churchyard, A., Velakoulis, D., Roxburgh, R. H., & Delatycki, M. B. (2010) · Movement Disorders · doi:10.1002/mds.23108 · Cited by 109
IRS2 increases mitochondrial dysfunction and oxidative stress in a mouse model of Huntington disease
Sadagurski, M., Cheng, Z., Rozzo, A., Palazzolo, I., Kelley, G. R., Dong, X., Krainc, D., & White, M. F. (2011) · Journal of Clinical Investigation · doi:10.1172/jci46305 · Cited by 107
“Moreover, calorie restriction extends the survival of polyQ-HTT mutant mice, which suggests that it can protect against neurodegeneration (17).”
Mo, C., Hannan, A. J., & Renoir, T. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.03.003 · Cited by 108
Structural and Functional Rescue of Chronic Metabolically Stressed Optic Nerves through Respiration
Harun‐Or‐Rashid, M., Pappenhagen, N., Palmer, P. G., Smith, M. A., Gevorgyan, V., Wilson, G. N., Crish, S. D., & Inman, D. M. (2018) · Journal of Neuroscience · doi:10.1523/jneurosci.3652-17.2018 · Cited by 104
“, 2002) and slow neurodegenerative disease progression (Duan et al., 2003).”
BackgroundGeisler, J. G. (2019) · Cells · doi:10.3390/cells8030280 · Cited by 104
Neuroprotective effects of dietary restriction: Evidence and mechanisms
Pani, G. (2015) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2015.03.004 · Cited by 103
Nature, nurture and neurology: gene–environment interactions in neurodegenerative disease
Spires‐Jones, T. L., & Hannan, A. J. (2005) · FEBS Journal · doi:10.1111/j.1742-4658.2005.04677.x · Cited by 102
The substrates of memory: Defects, treatments, and enhancement
LYNCH, G. S., Rex, C. S., Chen, L. Y., & Gall, C. M. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2007.11.082 · Cited by 103
“Both patients and the mice are reported to have reduced BDNF levels (Duan et al., 2003; Ferrer et al., 2000; Zuccato et al., 2001), something that could lead to deficits in spine actin polymerization and thus LTP consolidation (see Fig 4).”
BackgroundXu, X. Z. S., Zhan, M., Duan, W., Prabhu, V. V., Brenneman, R., Wood, W. H., Firman, J., Li, H., Zhang, P., Ibe, C. N., et al. (2007) · Genome biology · doi:10.1186/gb-2007-8-11-r234 · Cited by 100
“Most of the striatal age-related changes were reverted by CR, an anti-aging intervention shown to protect neurons in a mouse model of Huntington's disease [25] and a monkey model of Parkinson's disease [26], suggesting that they may be fundamental to the aging process.”
BackgroundSelf-citationMacDonald, M. E., Ginés, S., Gusella, J. F., & Wheeler, V. C. (2003) · NeuroMolecular Medicine · doi:10.1385/nmm:4:1-2:7 · Cited by 104
“, 2002) or with calorie restriction (Duan et al., 2003).”
BackgroundChallenging Oneself Intermittently to Improve Health
Mattson, M. P. (2014) · Dose-Response · doi:10.2203/dose-response.14-028.mattson · Cited by 98
“Numerous studies have shown that BDNF can protect neurons against degeneration and death in experimental models relevant to the pathogenesis of Alzheimer’s, Parkinson’s and Huntington’s diseases (Duan et al., 2003; Zuccato and Cattaneo, 2009; Intlekofer and Cotman, 2013).”
BackgroundInfluentialSelf-citationA forkhead in the road to longevity: the molecular basis of lifespan becomes clearer
Morris, B. J. (2005) · Journal of Hypertension · doi:10.1097/01.hjh.0000173509.45363.dd · Cited by 98
Chiang, M.-C., Chen, H.-M., Lee, Y.-H., Chang, H.-H., Wu, Y.-C., Soong, B.-W., Chen, C.-M., Wu, Y.-R., Liu, C.-S., Niu, D.-M., et al. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddl481 · Cited by 95
Chiang, M., Chen, C., Lee, M.-R., Chen, H.-W., Chen, H., Wu, Y.-S., Hung, C.-H., Kang, J.-J., Chang, C., Chang, C., et al. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq322 · Cited by 98
“Importantly, amelioration of hyperglycemia is associated with improvement of the neurological deficits of HD (21).”
BackgroundWang, H. B., Loh, D. H., Whittaker, D. S., Cutler, T., Howland, D., & Colwell, C. S. (2018) · eNeuro · doi:10.1523/eneuro.0431-17.2017 · Cited by 95
“In the HD-N171-82Q mouse model, CR improves motor performance and survival while reducing cell death (Duan et al., 2003).”
Aziz, N. A. (2007) · Reviews in the Neurosciences · doi:10.1515/revneuro.2007.18.3-4.223 · Cited by 94
Fasting as a Therapy in Neurological Disease
Phillips, M. C. L. (2019) · Nutrients · doi:10.3390/nu11102501 · Cited by 99
Zuccato, C., & Cattaneo, E. F. (2014) · Handbook of experimental pharmacology · doi:10.1007/978-3-642-45106-5_14 · Cited by 94
“BDNF levels have also been tested in N171-82Q mice produced by David Borchelt laboratory at Johns Hopkins University and expressing a 517 amino acid N-terminal portion of huntingtin with 82 glutamine repeats driven by a mouse prion protein promoter (Duan et al. 2003; Schilling et al. 1999).”
BackgroundMethodThe impact of dietary energy intake on cognitive aging
Mattson, M. P. (2010) · Frontiers in Aging Neuroscience · doi:10.3389/neuro.24.005.2010 · Cited by 91
Self-citationParoxetine retards disease onset and progression in Huntingtin mutant mice
Duan, W., Guo, Z., Jiang, H., Ladenheim, B., Xu, X. Z. S., Cadet, J. L., & Mattson, M. P. (2004) · Annals of Neurology · doi:10.1002/ana.20075 · Cited by 91
“We previously reported that the HD mice exhibit progressive weight loss.(9) HD mice given paroxetine lost weight at a significantly slower rate than did vehicle-treated HD mice (see Fig 1C).”
BackgroundMethodInfluentialSelf-citationMood disorders in Huntington's disease: from behavior to cellular and molecular mechanisms
Pla, P., Orvoën, S., Saudou, F., David, D. J. P., & Humbert, S. (2014) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2014.00135 · Cited by 97
“Male subjects = 47%”
An Evolutionary Perspective on Why Food Overconsumption Impairs Cognition
Mattson, M. P. (2019) · Trends in Cognitive Sciences · doi:10.1016/j.tics.2019.01.003 · Cited by 94
Self-citationSirtuins: from metabolic regulation to brain aging
Duan, W. (2013) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2013.00036 · Cited by 89
“Our previous study showed that CR could ameliorate the motor phenotype and extend survival of HD mice (Duan et al., 2003), indicating that pathways related to energy metabolism can modify disease progression in the disease.”
BackgroundSelf-citationAgeing and metabolism: drug discovery opportunities
Curtis, R., Geesaman, B. J., & DiStefano, P. S. (2005) · Nature Reviews Drug Discovery · doi:10.1038/nrd1777 · Cited by 86
Giampà, C., Montagna, E., Dato, C., Melone, M. A. B., Bernardi, G., & Fusco, F. R. (2013) · PLoS ONE · doi:10.1371/journal.pone.0064037 · Cited by 87
Circadian Influences of Diet on the Microbiome and Immunity
Zheng, D., Ratiner, K., & Elinav, E. (2020) · Trends in Immunology · doi:10.1016/j.it.2020.04.005 · Cited by 88
“In HD-N171-82Q mutant mice (a model for Huntington ’ s disease), ADF slows disease onset and improves the survival of these mice by normalizing blood glucose and brain-derived neurotrophic factor [141].”
Zhao, Y., Jia, M., Chen, W., & Liu, Z. (2022) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2022.02.021 · Cited by 89
Intermittent Fasting Improves Functional Recovery after Rat Thoracic Contusion Spinal Cord Injury
Jeong, M., Plunet, W. T., Streijger, F., Lee, J. H. T., Plemel, J. R., Park, S., Lam, C. K., Liu, J., & Tetzlaff, W. (2011) · Journal of Neurotrauma · doi:10.1089/neu.2010.1609 · Cited by 84
“…Sharma and Kaur, 2005), stroke (Yu and Mattson, 1999), Parkinson’s disease (Maswood et al., 2004), Huntington’s disease (Bruce-Keller et al., 1999; Duan et al., 2003), and Alzheimer’s disease (Halagappa et al., 2007; Mouton et al., 2009; Patel et al., 2005; Qin et al., 2006; Wang et al., 2005; Wu…”
Ehrnhoefer, D. E., Martin, D. D. O., Schmidt, M. E., Qiu, X., Ladha, S., Caron, N. S., Skotte, N. H., Nguyen, Y. T. N., Vaid, K., Southwell, A. L., et al. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0518-0 · Cited by 81
“These results provide a potential molecular mechanism for the beneficial effects of nutrient deprivation on neurodegenerative diseases [15, 31, 38, 54] and demonstrate that autophagy pathways that are not impacted by the HD pathology can be harnessed to lower mHTT protein levels in vivo.”
BackgroundThe neuropathology of obesity: insights from human disease
Lee, E. B., & Mattson, M. P. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1190-x · Cited by 84
“IF can also increase the survival of neurons arising from stem cells in the hippocampus [140] and can preserve function of neurons in animal models of AD, Parkinson’s disease and Huntington’s diseases [67, 69, 106].”
Self-citationThe need for controlled studies of the effects of meal frequency on health
Mattson, M. P. (2005) · The Lancet · doi:10.1016/s0140-6736(05)66667-6 · Cited by 77
Self-citationSchellinck, H. M., Cyr, D. P., & Brown, R. E. (2010) · Advances in the study of behavior · doi:10.1016/s0065-3454(10)41007-4 · Cited by 80
“, 2009); delayed neural atrophyand improvesmotor performanceon the rotarod in theHD-N171-82Q mousemodel ofHuntington’s disease (Duan et al., 2003); reduced anxiety and improved motor behavior in the Mecp2308/y mouse model of Rett syndrome (Mantis et al.”
BackgroundCognitive Dysfunction in Huntington's Disease: Humans, Mouse Models and Molecular Mechanisms
Giralt, A., Saavedra, A., Alberch, J., & Pérez‐Navarro, E. (2012) · Journal of Huntington s Disease · doi:10.3233/jhd-120023 · Cited by 78
Translating therapies for Huntington’s disease from genetic animal models to clinical trials
Hersch, S. M., & Ferrante, R. J. (2004) · NeuroRx · doi:10.1602/neurorx.1.3.298 · Cited by 75
“Interestingly, dietary restriction of these mice improves survival by about 2 weeks.(11) Transgenic mice with full-length huntingtin containing 48 or 89 CAG repeats have been described that show behavioral abnormalities and neuron loss(12) but have not been available for use in therapeutic discovery.”
Early defect of transforming growth factor β1 formation in Huntington’s disease
Battaglia, G., Cannella, M., Riozzi, B., Orobello, S., Maat–Schieman, M. L. C., Aronica, E., Busceti, C. L., Ciarmiello, A., Alberti, S., Amico, E., et al. (2010) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2010.01011.x · Cited by 71
“In addition, strategies that increase brain levels of BDNF or glial-derived neurotrophic factor (GDNF) are neuroprotective in HD models [36, 48–58].”
BackgroundEffect of caloric restriction on depression
Manchishi, S. M., Cui, R., Zou, X. H., Cheng, Z. Q., & Li, B. J. (2018) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.13418 · Cited by 71
The role of calorie restriction and SIRT1 in prion-mediated neurodegeneration
Chen, D., Steele, A. D., Hütter, G., Bruno, J., Govindarajan, A., Easlon, E. J., Lin, S.-J., Aguzzi, A., Lindquist, S. L., & Guarente, L. (2008) · Experimental Gerontology · doi:10.1016/j.exger.2008.08.050 · Cited by 74
“However, CR dramatically delays all aspects of Huntington’s disease, in which weight loss and a disruption of energy balance are apparent (Duan et al., 2003).”
BackgroundResultInfluentialFasting: From Physiology to Pathology
Tang, D., Tang, Q., Huang, W., Zhang, Y., Tian, Y., & Fu, X. (2023) · Advanced Science · doi:10.1002/advs.202204487 · Cited by 74
Srivastava, S., & Haigis, M. C. (2011) · Current Pharmaceutical Design · doi:10.2174/138161211798072526 · Cited by 70
Stoyas, C. A., Bushart, D. D., Switonski, P. M., Ward, J. M., Alaghatta, A., Tang, M., Niu, C., Wadhwa, M., Huang, H., Savchenko, A., et al. (2019) · Neuron · doi:10.1016/j.neuron.2019.11.019 · Cited by 69
“Sirtuins can promote lifespan, and as caloric restriction in mouse models of neurodegeneration yields amelioration of disease (Duan et al., 2003; Halagappa et al., 2007; Patel et al., 2005; Wang et al., 2005), Sirt1 can achieve neuroprotection in Huntington’s disease (Jeong et al.”
BackgroundExercise is not beneficial and may accelerate symptom onset in a mouse model of Huntington’s disease
Potter, M. C., Yuan, C., Ottenritter, C., Mughal, M. R., & van Praag, H. (2010) · PLoS Currents · doi:10.1371/currents.rrn1201 · Cited by 68
“Deficits in locomotor activity are a hallmark of HD [15] [17] [18] [19] [20] .”
BackgroundInfluentialGinés, S., Paoletti, P., & Alberch, J. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.084202 · Cited by 68
Cholesterol dysfunction in neurodegenerative diseases: Is Huntington's disease in the list?
Valenza, M., & Cattaneo, E. F. (2006) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2006.09.005 · Cited by 71
Sharma, S., & Kaur, G. (2005) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2005.07.015 · Cited by 67
Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein
Al‐Ramahi, I., Giridharan, S. S. P., Chen, Y., Patnaik, S., Safren, N., Hasegawa, J., de Haro, M., Gee, A. K. W., Titus, S. A., Jeong, H., et al. (2017) · eLife · doi:10.7554/elife.29123 · Cited by 70
“Note that caloric restriction also raises the basal level of autophagy, leading to improvements in HD models (Duan et al., 2003) and increasing axonal autophagosome transport (Ikenaka et al.”
BackgroundEnvironmental enrichment affects striatal graft morphology and functional recovery
Döbrössy, M. D., & Dunnett, S. B. (2004) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2004.03105.x · Cited by 66
Systemic manifestation and contribution of peripheral tissues to Huntington’s disease pathogenesis
Chuang, C.-L., & Demontis, F. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2021.101358 · Cited by 66
Hu, Y., Zhang, M., Chen, Y., Yang, Y., & Zhang, J. (2018) · European Journal of Nutrition · doi:10.1007/s00394-018-1606-4 · Cited by 65
Turi, G. (2003) · Florence Research (University of Florence) · Cited by 69
Metabolic and molecular framework for the enhancement of endurance by intermittent food deprivation
Marosi, K., Moehl, K., Navas‐Enamorado, I., Mitchell, S. J., Zhang, Y., Lehrmann, E., Aon, M. A., Cortassa, S. C., Becker, K. G., & Mattson, M. P. (2018) · The FASEB Journal · doi:10.1096/fj.201701378rr · Cited by 62
Self-citationBarriga, G. G.-D., Giralt, A., Anglada‐Huguet, M., Gaja‐Capdevila, N., Orlandi, J. G., Soriano, J., Canals, J. M., & Alberch, J. (2017) · Human Molecular Genetics · doi:10.1093/hmg/ddx198 · Cited by 68
“In support of this view, BDNF levels are abnormally low in brain tissue from both human HD patients, (7,16) and murine HD models (17,18).”
BackgroundInhibitors of metabolism rescue cell death in Huntington's disease models
Varma, H., Cheng, R., Voisine, C., Hart, A. C., & Stockwell, B. R. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0704482104 · Cited by 61
Mattson, M. P. (2014) · Journal of Parkinson s Disease · doi:10.3233/jpd-130335 · Cited by 60
“Intermittent fasting (alternate day food deprivation) protected hippocampal neurons against synaptic dysfunction in a transgenic mouse model of AD [54], in rat and mouse models of HD [55] [56] and in a mouse model of focal ischemic stroke [57].”
Self-citationMouse Models of Polyglutamine Diseases: Review and Data Table. Part I
Figiel, M., Szlachcic, W. J., Switonski, P. M., Gabka, A., & Krzyżosiak, W. J. (2012) · Molecular Neurobiology · doi:10.1007/s12035-012-8315-4 · Cited by 60
“N171-82Q mice exhibit progressive neurodegeneration that manifests in brain atrophy [77–80] and reactive gliosis [52].”
BackgroundGenetic and environmental factors in the pathogenesis of Huntington’s disease
van Dellen, A., & Hannan, A. J. (2004) · Neurogenetics · doi:10.1007/s10048-003-0169-5 · Cited by 59
van Dellen, A., Grote, H., & Hannan, A. J. (2005) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2005.04313.x · Cited by 60
Synaptopathic mechanisms of neurodegeneration and dementia: Insights from Huntington’s disease
Tyebji, S., & Hannan, A. J. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.03.008 · Cited by 62
“…Zuccato et al., 2001; Gauthier et al., 2004) and transgenic HD mice (Zuccato et al., 2001, 2003; LuthiCarter et al., 2002; Gines et al., 2003, 2006; Duan et al., 2003; Zhang et al., 2003; Spires et al., 2004b; Hermel et al., 2004; Gauthier et al., 2004; Pang et al., 2006; for review see Zuccato…”
Gutierrez, A. M., Corey‐Bloom, J., Thomas, E. A., & Desplats, P. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2019.00335 · Cited by 58
Rich, N. J., Landingham, J. W. V., Figueiroa, S., Seth, R., Corniola, R. S., & Levenson, C. W. (2010) · Journal of Neuroscience Research · doi:10.1002/jnr.22443 · Cited by 57
“…to attenuate the neuronal degeneration and behavioral deficits associated with rodent (Duan and Mattson, 1999) and primate (Maswood et al., 2004) models of Parkinson’s disease, as well as slow disease progression in the huntingtin mutant mouse model of Huntington’s disease (Duan et al., 2003).”
BackgroundImpaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease
Texel, S. J., & Mattson, M. P. (2010) · Antioxidants and Redox Signaling · doi:10.1089/ars.2010.3569 · Cited by 58
“Activation of adaptive stress responses in animal models of neurodegenerative diseases have been able to provide benefits in cognition and motor function, and suggest that these molecular pathways maybe able to be activated through cognitive stimulation, exercise, and CR (41, 42, 67, 76, 108, 125).”
BackgroundSelf-citationHypothalamic gene transfer of BDNF promotes healthy aging in mice
McMurphy, T. B., Huang, W., Liu, X., Siu, J. J., Queen, N. J., Xiao, R., & Cao, L. (2018) · Aging Cell · doi:10.1111/acel.12846 · Cited by 55
Insulin and Autophagy in Neurodegeneration
de Mello, N. P., Orellana, A. M., Mazucanti, C. H., Lima, G. D. M., Scavone, C., & Kawamoto, E. M. (2019) · Frontiers in Neuroscience · doi:10.3389/fnins.2019.00491 · Cited by 57
“, 2006), dietary restriction in a HD mouse model resulted in an increase in autophagy and a reduction in mHtt aggregate formation and the normalization of blood glucose regulation, thereby contributing to a slower disease progression and an extended lifespan (Duan et al., 2003; Ehrnhoefer et al., 2018).”
BackgroundWilson, K. A., Chamoli, M., Hilsabeck, T. A. U., Pandey, M., Bansal, S., Chawla, G., & Kapahi, P. (2021) · Cell Metabolism · doi:10.1016/j.cmet.2021.08.018 · Cited by 57
“DR also improves neurotrophic factors and stress response in mice (Duan et al., 2003) as well as DNA maintenance in mice with DNA repair deficiencies (Ercc1Δ/− and Ercc5−/−) (Vermeij et al.”
BackgroundBastani, A., Rajabi, S., & Kianimarkani, F. (2017) · Neurology International · doi:10.4081/ni.2017.7043 · Cited by 55
Caloric restriction does not reverse aging-related changes in hippocampal BDNF
Newton, I. G., Forbes, M. E., Legault, C., Johnson, J. E., Brunso‐Bechtold, J. K., & Riddle, D. R. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2004.06.005 · Cited by 55
DNA methylation and cognitive aging
Xu, X. Z. S. (2015) · Oncotarget · doi:10.18632/oncotarget.4215 · Cited by 57
“Favorable interventions such as dietary restriction, physical exercise, and enriched environment have been identified as potential means to slow brain ageing and forestall neurodegeneration and cognition, and act in part by increasing BDNF expression and enhancing neurogenesis in hippocampus [28-32].”
BackgroundDrug Delivery Systems for the Treatment of Ischemic Stroke
Rhim, T., Lee, D. Y., & Lee, M. (2013) · Pharmaceutical Research · doi:10.1007/s11095-012-0959-2 · Cited by 54
“Increasing innate BDNF levels by stimulating BDNF expression has been shown to improve diseases in several Huntington’s disease (HD) mouse models (43,44).”
BackgroundSirtuin 1 activator SRT 2104 protects Huntington's disease mice
Jiang, M., Zheng, J., Peng, Q., Hou, Z., Zhang, J., Mori, S., Ellis, J. L., Vlasuk, G. P., Fries, H. E., Suri, V., et al. (2014) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.135 · Cited by 54
“Male mice were used in our studies as reported previously.(13) SRT2104 (>98% purity) was synthesized by Sirtris, a GlaxoSmithKline company.”
MethodSelf-citationGalas, M., Bizat, N., Cuvelier, L., Bantubungi, K., Brouillet, E., Schiffmann, S. N., & Blum, D. L. (2003) · Neurobiology of Disease · doi:10.1016/j.nbd.2003.09.013 · Cited by 54
“, 2001) through, for example, the lack of trophic support afforded by the cortical synthesis of BDNF (Duan et al., 2003; Laforet et al., 2001).”
BackgroundDietary Restriction and Neuroinflammation: A Potential Mechanistic Link
Bok, E., Jo, M., Lee, S., Lee, B.-R., Kim, J., & Kim, H.-J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20030464 · Cited by 53
“DR also attenuated pathologic events in a mouse model of Huntington’s disease (HD) [136].”
BackgroundTargeting Sirtuin-1 in Huntington’s Disease: Rationale and Current Status
Duan, W. (2013) · CNS Drugs · doi:10.1007/s40263-013-0055-0 · Cited by 54
Self-citationCrocker, S. F., Costain, W. J., & Robertson, H. A. (2006) · Brain Research · doi:10.1016/j.brainres.2006.02.102 · Cited by 52
Huntington’s Disease and Diabetes: Chronological Sequence of its Association
Montojo, M. T., Aganzo, M., & González, N. (2017) · Journal of Huntington s Disease · doi:10.3233/jhd-170253 · Cited by 52
“and muscle were detected in HdhCAG(150) mice, suggesting a potential connection with metabolism [36, 37].”
BackgroundArbez, N., Ratovitski, T., Roby, E., Chighladze, E., Stewart, J. C., Ren, M., Wang, X., Lavery, D. J., & Ross, C. A. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.782300 · Cited by 52
Tiagabine is neuroprotective in the N171-82Q and R6/2 mouse models of Huntington's disease
Masuda, N., Peng, Q., Li, Q., Jiang, M., Liang, Y., Wang, X., Zhao, M., Wang, W., Ross, C. A., & Duan, W. (2008) · Neurobiology of Disease · doi:10.1016/j.nbd.2008.01.014 · Cited by 51
“We used male N171-82Q HD mice for all our studies since we found that there is significant variability in all phenotypes between male and female N171-82Q mice (Duan et al., 2003).”
MethodSelf-citationLee, J., Kim, S. J., Son, T. G., Chan, S. L., & Mattson, M. P. (2006) · Journal of Neuroscience Research · doi:10.1002/jnr.20831 · Cited by 50
“In addition, IF can reduce neuronal damage and improve functional outcome in animal models of stroke (Yu and Mattson, 1999), Parkinson’s disease (Duan and Mattson, 1999), and Huntington’s disease (Duan et al., 2003).”
BackgroundInfluentialSelf-citationJin, J., Gu, H., Anders, N. M., Ren, T., Jiang, M., Tao, M., Peng, Q., Rudek, M. A., & Duan, W. (2016) · NeuroMolecular Medicine · doi:10.1007/s12017-016-8412-z · Cited by 50
“We have shown that CR delayed onset and slowed disease progression in a mouse model of HD and other neurodegenerative diseases (Duan et al. 2003).”
Ibrahim, W. W., & Rasheed, N. O. A. (2022) · Inflammopharmacology · doi:10.1007/s10787-022-01004-z · Cited by 50
“It was previously reported that BDNF protein levels are reduced in HD animal models (Ferrer et al. 2000; Duan et al. 2003).”
BackgroundThe Effects of Dietary Interventions on Brain Aging and Neurological Diseases
Lobo, F., Haase, J., & Brandhorst, S. (2022) · Nutrients · doi:10.3390/nu14235086 · Cited by 54
Huntington’s Disease Does Not Appear to Increase the Risk of Diabetes Mellitus
Boesgaard, T. W., Nielsen, T. T., Josefsen, K. E., Hansen, T. F., Jørgensen, T., Pedersen, O. B., Nørremølle, A., Nielsen, J., & Hasholt, L. (2009) · Journal of Neuroendocrinology · doi:10.1111/j.1365-2826.2009.01898.x · Cited by 50
Moreno, C. L., & Mobbs, C. V. (2016) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2016.11.013 · Cited by 50
Williams, W. M., Castellani, R. J., Weinberg, A., Perry, G. L., & Smith, M. A. (2012) · The Scientific World JOURNAL · doi:10.1100/2012/905785 · Cited by 47
“Attenuation in function may be attributed to an a priori development of an insidious condition, such as hyperglycemia and/or increased insulin resistance, a component of many neuropathological conditions including AD [26], Huntington’s disease [27], aging of the brain [28], diabetes mellitus [29, 30], and TBI [31].”
BackgroundWu, B., Jiang, M., Peng, Q., Li, G., Hou, Z., Milne, G. L., Mori, S., Alonso, R. J., Geisler, J. G., & Duan, W. (2017) · Experimental Neurology · doi:10.1016/j.expneurol.2017.03.020 · Cited by 46
“We have demonstrated that HD mice maintained on a DR regimen exhibited significantly improved motor function and lessened brain pathology (Duan et al., 2003).”
Self-citationHolmer, H. K., Keyghobadi, M., Moore, C., Menashe, R. A., & Meshul, C. K. (2005) · Synapse · doi:10.1002/syn.20163 · Cited by 47
“…in several models of neurodegeneration, including druginduced and aging (Anson et al., 2003; Bruce-Keller et al., 1999; Duan and Mattson, 1999; Duan et al., 2003; Eckles-Smith et al., 2000; Sohal et al., 1994; Sohal and Weindruch, 1996; Wachsman, 1996), the primary question in the current…”
Background
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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