Oliver von Bohlen und HalbachEditorial on the Research Topic
Cellular and molecular responses to changes in nutrition and exercise
Neurological and neuropsychiatric disorders pose a significant burden on human health and society throughout the world. In the past 30 years, the absolute numbers of deaths and people with disabilities owing to neurological diseases have risen substantially (Feigin et al., 2020). The prevalence of overweight and obesity has also increased in the last decades worldwide (Ng et al., 2014). In this context it is important to note that obesity has been associated with a higher risk for developing neuropsychiatric disorders. For example, in a recent Swedish study, about half of all young people treated for severe obesity have neuropsychiatric problems (Bjork et al., 2021). In addition, obesity has been shown to be associated with declines in cognitive performance in humans. Thus, a higher body mass index (BMI) is associated with lower cognitive scores and a higher BMI at baseline is associated with a higher cognitive decline at follow-up (Cournot et al., 2006). Leptin-deficient (ob/ob; an animal model of obesity) mice display altered adult hippocampal neurogenesis (Bracke et al., 2019). In addition, leptin-receptor deficient (db/db, a further animal model of obesity) mice also show impairments in adult hippocampal neurogenesis (Ramos-Rodriguez et al., 2014) and disturbances in cognitive functions (Ramos-Rodriguez et al., 2013).
Dietary restriction can help reduce excess adipose tissue and obesity. Moreover, dietary restriction can increase life span in a wide variety of species, and may also promote neuronal survival. Various studies hint that nutrition has an impact on brain functions. Among others, dietary restriction has beneficial effects on neuronal plasticity, adult hippocampal neurogenesis and cognitive functions. Increasing energy expenditure can also help to reduce or balance body weight. Energy expenditure can, among others, be increased by increasing physical activity. Physical exercise is thought to play an important role in the prevention and delayed progression of neurological disease through a variety of cellular and molecular mechanisms. Indeed, an association between physical activity and mental health has been reported (see for details: Biddle and Asare, 2011; Lubans et al., 2016). Physical exercise, especially running, has effects on the brain morphology, including increased hippocampal volume (Biedermann et al., 2016). Exercise has profound effects on adult hippocampal neurogenesis and hippocampus-dependent learning (van Praag et al., 1999). Several molecular systems seemed to be important for maintaining neuronal function and plasticity in this context. Among these factors, the neurotrophins, especially, brain-derived neurotrophic factor (BDNF) plays a prominent role (Vivar et al., 2013). Mice deficient for BDNF indeed show altered hippocampal functions (von Bohlen und Halbach, 2010) and are getting obese over time (Kernie et al., 2000). Likewise, in humans, polymorphism in the BDNF gene (Val66Met) has been associated with obesity (Skledar et al., 2012). Moreover, an association of the Val66Met BDNF polymorphism with reduced hippocampal volumes in major depression has been reported (Frodl et al., 2007). Thus, nutrition and exercise can have a strong impact upon neuronal functions and neuronal plasticity. Whilst there is a growing body of work studying the effects of energy metabolism on the functions of the brain, there are still many unanswered questions on the mechanisms that underlie these changes and their potential role in disease prevention.
Two articles report about further molecules that are involved in regulating physical exercise stimulated adult hippocampal neurogenesis, namely the cyclin-dependent kinase inhibitor p16Ink4a (Micheli et al.) and adiponectin (Wang et al.). Ge and Dai report about the effects of 3-week treadmill exercise on the electrophysiological and channel properties of serotonergic neurons located in the dorsal raphe nucleus. In the paper by Liśkiewicz et al. it is analyzed whether stimulation of autophagy is one of the mediators of ketogenic diet induced neuroprotection in the hippocampus.
This Research Topic aimed to bring about new findings on the cellular and molecular processes that impact brain function in health and disease. The data presented here mainly focus on the beneficial role of ketonic diet and physical exercise on brain function, including the effects on neuronal circuitries and neuronal plasticity. Taken together, the articles support the view that the balance between nutrition and exercise is of paramount importance for cognitive health and the maintenance of brain structures.
Author contributions
The author confirms being the sole contributor of this work and has approved it for publication.
Conflict of interest
The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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References
Biddle, S. J., and Asare, M. (2011). Physical activity and mental health in children and adolescents: a review of reviews. Br. J. Sports Med. 45, 886–895 doi: 10.1136/bjsports-2011-090185
Biedermann, S. V., Fuss, J., Steinle, J., Auer, M. K., Dormann, C., Falfan-Melgoza, C., et al. (2016). The hippocampus and exercise: histological correlates of mr-detected volume changes. Brain Struct. Funct. 221, 1353–1363 doi: 10.1007/s00429-014-0976-5
Bjork, A., Dahlgren, J., Gronowitz, E., Henriksson Wessely, F., Janson, A., Engstrom, M., et al. (2021). High prevalence of neurodevelopmental problems in adolescents eligible for bariatric surgery for severe obesity. Acta Paediatr. 110, 1534–1540 doi: 10.1111/apa.15702
Bracke, A., Domanska, G., Bracke, K., Harzsch, S., van den Brandt, J., Broker, B., et al. (2019). Obesity impairs mobility and adult hippocampal neurogenesis. J. Exp. Neurosci. 13, 1179069519883580. doi: 10.1177/1179069519883580
Cournot, M., Marquie, J. C., Ansiau, D., Martinaud, C., Fonds, H., Ferrieres, J., et al. (2006). Relation between body mass index and cognitive function in healthy middle-aged men and women. Neurology 67, 1208–1214 doi: 10.1212/01.wnl.0000238082.13860.50
Feigin, V. L., Vos, T., Nichols, E., Owolabi, M. O., Carroll, W. M., Dichgans, M., et al. (2020). The global burden of neurological disorders: translating evidence into policy. Lancet Neurol. 19, 255–265 doi: 10.1016/S1474-4422(19)30411-9
Frodl, T., Schule, C., Schmitt, G., Born, C., Baghai, T., Zill, P., et al. (2007). Association of the brain-derived neurotrophic factor val66met polymorphism with reduced hippocampal volumes in major depression. Arch. Gen. Psychiatry 64, 410–416 doi: 10.1001/archpsyc.64.4.410
Kernie, S. G., Liebl, D. J., and Parada, L. F. (2000). Bdnf regulates eating behavior and locomotor activity in mice. EMBO J. 19, 1290–1300 doi: 10.1093/emboj/19.6.1290
Lubans, D., Richards, J., Hillman, C., Faulkner, G., Beauchamp, M., Nilsson, M., et al. (2016). Physical activity for cognitive and mental health in youth: a systematic review of mechanisms. Pediatrics 138, e20161642. doi: 10.1542/peds.2016-1642
Ng, M., Fleming, T., Robinson, M., Thomson, B., Graetz, N., Margono, C., et al. (2014). Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the global burden of disease study 2013. Lancet 384, 766–781 doi: 10.1016/S0140-6736(14)60460-8
Ramos-Rodriguez, J. J., Molina-Gil, S., Ortiz-Barajas, O., Jimenez-Palomares, M., Perdomo, G., Cozar-Castellano, I., et al. (2014). Central proliferation and neurogenesis is impaired in type 2 diabetes and prediabetes animal models. PLoS ONE 9, e89229doi: 10.1371/journal.pone.0089229
Ramos-Rodriguez, J. J., Ortiz, O., Jimenez-Palomares, M., Kay, K. R., Berrocoso, E., Murillo-Carretero, M. I., et al. (2013). Differential central pathology and cognitive impairment in pre-diabetic and diabetic mice. Psychoneuroendocrinology 38, 2462–2475 doi: 10.1016/j.psyneuen.2013.05.010
Skledar, M., Nikolac, M., Dodig-Curkovic, K., Curkovic, M., Borovecki, F., and Pivac, N. (2012). Association between brain-derived neurotrophic factor val66met and obesity in children and adolescents. Prog. Neuropsychopharmacol. Biol. Psychiatry 36, 136–140 doi: 10.1016/j.pnpbp.2011.08.003
van Praag, H., Christie, B. R., Sejnowski, T. J., and Gage, F. H. (1999). Running enhances neurogenesis, learning, and long-term potentiation in mice. Proc. Natl. Acad. Sci. U. S. A. 96, 13427–13431 doi: 10.1073/pnas.96.23.13427
Vivar, C., Potter, M. C., and van Praag, H. (2013). All about running: synaptic plasticity, growth factors and adult hippocampal neurogenesis. Curr. Top. Behav. Neurosci. 15, 189–210 doi: 10.1007/7854_2012_220
Keywords: exercise, neuronal plasticity, synaptic plasticity, adult neurogenesis, hippocampus, serotonin
Citation: von Bohlen und Halbach O (2022) Editorial: Cellular and molecular responses to changes in nutrition and exercise. Front. Cell. Neurosci. 16:1102308. doi: 10.3389/fncel.2022.1102308
Received: 18 November 2022; Accepted: 24 November 2022;
Published: 06 December 2022.
Edited and reviewed by: Arianna Maffei, Stony Brook University, United States
Copyright © 2022 von Bohlen und Halbach. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Oliver von Bohlen und Halbach, b2xpdmVyLnZvbmJvaGxlbiYjeDAwMDQwO3VuaS1ncmVpZnN3YWxkLmRl