{"title":"HIT Your Brain: Neuron and New Run.","authors":"Min-Chul Lee, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_18","DOIUrl":"10.1007/978-981-95-0066-6_18","url":null,"abstract":"<p><p>The importance of physical activity in neuroscience is gaining increasing recognition. The question arises: What is the specific focus of exercise, and what factors contribute to the observed benefits of exercise in neuroscience? Various forms of exercise have been examined across physiological, psychological, and biochemical experiments within neuroscience. Still, there is a need for greater clarity to identify optimal exercise conditions, including the FITT-VP variables (frequency, intensity, type, and time).This chapter aims to shed light on the positive impacts of high-intensity training (HIT) exercises in facilitating physiological adaptation and exploring the newfound role in brain functions. Key areas explored include (1) exercise neuroscience at the structural level involving synaptic plasticity and neurogenesis; (2) functional level concerning behavioral development; and (3) molecular level addressing potential mechanisms underlying exercise-induced brain plasticity.Overall, high-intensity training emerges as a more cost-effective method for enhancing physiological adaptations, including improvements in aerobic capacity. Additionally, it has been shown to influence brain functions such as hippocampus-dependent learning and memory positively. These findings offer valuable insights into the practicality of high-intensity training for performance improvement and suggest directions for future research.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"335-341"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Potential Role of Extracellular Vesicles in Mediating Effects of Exercise on Brain Function.","authors":"Hyo Youl Moon, Henriette van Praag","doi":"10.1007/978-981-95-0066-6_8","DOIUrl":"10.1007/978-981-95-0066-6_8","url":null,"abstract":"<p><p>Exercise has a remarkable capacity to improve brain function by fostering neuronal plasticity, which enables us to better cope with various psychological and cognitive challenges. Numerous studies have demonstrated the neuroprotective effects of exercise. However, the underlying molecular mechanisms of the neuroprotective effects of exercise are not yet fully understood. In particular, the role of exercise-induced secretion of peripheral factors into circulation that influence the brain is understudied. Recent research has shown that extracellular vesicles (EVs), including microvesicles (MVs) and exosomes, are secreted during exercise. The discovery that EVs can mediate intracellular communication by delivering cargo signifies a promising area of research to understand the impact of exercise on the brain. In the present review, we provide an overview of recent advancements in understanding the regulatory mechanisms of EV biogenesis and discuss how EV molecular composition is influenced by exercise. Additionally, we highlight the potential role of EVs as exercise-specific mediators and as a promising therapeutic tool for neurodegenerative diseases, such as Alzheimer's disease.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"161-174"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Substrate Binding and Conformational Dynamics of the Monoamine Transporters.","authors":"Jeppe C Nielsen, Claus J Loland","doi":"10.1007/978-3-031-96364-3_2","DOIUrl":"https://doi.org/10.1007/978-3-031-96364-3_2","url":null,"abstract":"<p><p>The monoamine transporters move substrates across the plasma membrane by an alternating-access mechanism, in which a central substrate-binding site is alternately exposed to either the extracellular milieu or the cytoplasm at any given time. This process is driven by co-transport of sodium ions along the inwardly directed sodium gradient. Alternating access to the central substrate-binding site is facilitated by a stepwise series of changes to the transporter conformation, referred to as the transport cycle. The focus of this chapter is to discuss the conformational dynamics of the monoamine transporters that are orchestrated by the binding of substrate and ions, as part of the transport cycle. Firstly, we describe the substrate-binding event, and how it is fine-tuned to induce the conformational flexibility needed to initiate transport. Secondly, we discuss how sodium fuels the substrate transport as well as how it is aided by potassium and chloride. We also provide a mechanistic description of the cooperativity of the two sodium-binding sites and how they couple allosterically to the intracellular gating mechanism. Thirdly, we go over the amino acid residues of the intra- and extracellular gates and how they affect the transporter conformation.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"46 ","pages":"35-62"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Development of Oligodendroglia and Myelin.","authors":"Hao Huang, Xiaofeng Xu, Mengsheng Qiu","doi":"10.1007/978-3-031-87919-7_3","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_3","url":null,"abstract":"<p><p>Myelin sheaths formed by oligodendrocytes (OLs) wrap around neuronal axons and allow for saltatory conduction of nerve impulses, significantly increasing the speed of electrical signal transmission. The development of oligodendrocyte lineage consists of several coordinated steps. Briefly, oligodendrocyte precursor cells (OPCs) are first generated from neural precursor cells of certain neuroepithelial regions, and then they proliferate and migrate to other regions of the central nervous system (CNS), where they differentiate into oligodendrocytes and form myelin sheaths around the axons of neurons. These developmental processes are tightly and precisely regulated during animal development by a cohort of intracellular molecular and extracellular signals.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"61-79"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ai Guo, Yuzhen Wei, Alexei Verkhratsky, Fu-Dong Shi
{"title":"Oligodendroglia in Neuromyelitis Optica Spectrum Disorder.","authors":"Ai Guo, Yuzhen Wei, Alexei Verkhratsky, Fu-Dong Shi","doi":"10.1007/978-3-031-87919-7_16","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_16","url":null,"abstract":"<p><p>Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory autoimmune disease of the central nervous system, in which aquaporin-4 immunoglobulin G (AQP4-IgG) targets the water channel aquaporin-4 (AQP4) localized at astrocytic endfeet, thus triggering inflammatory lesions and tissue damage. The pathological characteristics of NMOSD are early loss of oligodendrocytes, extensive demyelination, and axonal injury. The pathogenesis of oligodendrocyte damage in NMOSD includes complement-dependent bystander effect, antibody-dependent cell-mediated cytotoxicity bystander effect, glutamate toxicity, connexin dysregulation, and blood-brain barrier disruption. Remyelination levels in acute NMOSD lesions are low.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"457-472"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pupil Dynamics Predict Exercise Brain Stimulation: An Overview of Exercise Pupillometry.","authors":"Ryuta Kuwamizu, Yudai Yamazaki, Kazuya Suwabe, Kenji Suzuki, Yoshiyuki Sankai, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_6","DOIUrl":"https://doi.org/10.1007/978-981-95-0066-6_6","url":null,"abstract":"<p><p>Proper physical activity, even at a very light intensity such as walking or slow running, improves brain health related to prefrontal executive function and hippocampal memory. However, the neural mechanism behind the cognitive enhancement that occurs during dynamic aerobic exercise is elusive and remains unclear in humans. Recently, pupillometry has been attracting attention as a kind of readout of the brain's ascending arousal mechanism, especially for brain noradrenergic and cholinergic system activation. Thus, to identify the neural mechanism behind the effects of very-light-intensity exercise, our recent work has focused on pupillometry during aerobic exercise, and we have successfully shown the efficacy of pupil dilation as a biological marker, even during very-light-/light-intensity exercise (below the ventilatory threshold). Interestingly, neuromelanin-MRI contrast in the LC, a marker of LC integrity, predicted the magnitude of exercise-induced pupil dilation and psychological arousal changes at the individual level. In addition, we have found that pupil dilation during exercise predicted the positive impact of acute very-light-/light-intensity exercise on prefrontal executive performance and hippocampal memory performance. The series of exercise pupillometry studies we will discuss here provides essential insights into the neural substrates of the advantages of exercise-induced brain stimulation in humans.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"113-131"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jonathan Zegarra-Valdivia, Estrella Fernandez de Sevilla, Jaime Pignatelli, Ignacio Torres Aleman
{"title":"Interoceptive Signaling by Circulating Insulin Like Growth Factor I and Neuroprotection by Exercise.","authors":"Jonathan Zegarra-Valdivia, Estrella Fernandez de Sevilla, Jaime Pignatelli, Ignacio Torres Aleman","doi":"10.1007/978-981-95-0066-6_12","DOIUrl":"https://doi.org/10.1007/978-981-95-0066-6_12","url":null,"abstract":"<p><p>Physical activity has been proven to be beneficial for brain function. Due to a lack of appropriate therapies for the majority of brain diseases, exercise has become a favored alternative to prevent and even treat several of these pathologies. Thus, the mechanisms underlying the neuroprotective actions of exercise are under intense scrutiny. Furthermore, since many patients afflicted with different neurological conditions are not able to perform exercise, development of pharmacological mimics based on knowledge of underlying cellular and molecular mechanisms is of therapeutic interest (Narkar VA, Downes M, Yu RT, Embler E, Wang YX, Banayo E, Cell 134:405-415, 2008). As part of these mechanisms, we will examine the role of insulin-like growth factor I (IGF-I), a pleiotropic neuroprotective signal, and one of the established mediators of the beneficial actions of exercise in the brain. Exercise stimulates the entrance of circulating IGF-I into the brain where it mediates pro-neurogenic, pro-cognitive, and mood modulatory effects known to be associated to exercise. Through its potent cytoprotective actions (anti-apoptotic, anti-oxidant, anti-inflammatory), IGF-I participates in reparative and homeostatic processes associated to exercise. We postulate that circulating IGF-I, a regulator of muscle and bone mass, forms part of an interoceptive system within a humoral branch informing the brain of muscle/bone mass. In this way, IGF-I conveys interoceptive signaling to brain areas involved in orchestrating physical activity to adapt them to available vigor, i.e., muscle strength. Because exercise engages the activity of many brain areas, neuroprotection by exercise-elicited entrance of circulating IGF-I is brain-wide.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"217-229"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neuroprotective and Neurotrophic Effects of Astaxanthin on the Brain.","authors":"Jang Soo Yook, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_17","DOIUrl":"https://doi.org/10.1007/978-981-95-0066-6_17","url":null,"abstract":"<p><p>Oxidative stress in the brain is associated with the development and progression of neurological disorders, posing antioxidant nutrients as an effective strategy for protecting neuronal cells and potentially slowing cognitive decline. Bioactive compounds from natural sources with antioxidant effects promote brain health. Among various natural compounds, astaxanthin (ASX), a potent red-pigment carotenoid found in various microorganisms and marine animals, is well recognized for its potential health benefits. In this review, we highlight the promising neuroprotective effects of ASX through cellular experiments and animal models. This review can provide novel insights on the therapeutic potential of ASX through its antioxidant, anti-inflammatory, and anti-apoptotic effects against neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. In addition to demonstrating the neurotrophic effects of ASX on structural and functional changes in hippocampal neuronal plasticity, this review also discusses its synergistic potential with other interventions, such as exercise.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"317-334"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Application of Minimum Exercise Model to the Hypoxic Environment.","authors":"Genta Ochi, Yuhki Yamada, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_20","DOIUrl":"10.1007/978-981-95-0066-6_20","url":null,"abstract":"<p><p>While moderate exercise has been demonstrated to enhance executive function, this beneficial effect may vary depending on the exercise environment. For instance, the decline in blood oxygen levels (hypoxemia) associated with ascent to high altitude has been shown not only to induce acute mountain sickness but also to potentially cause decreased cognitive performance. Therefore, exercise under hypoxic conditions may reduce oxygen delivery to various tissues, thereby attenuating the executive function-enhancing effects of exercise. Previous studies have examined the impact of exercise in hypoxic environments on cognitive function using cognitive task paradigms; however, a consensus has not been reached. One contributing factor to this lack of consensus is the insufficient investigation of how exercise in hypoxic environments affects neural activity in brain regions specific to cognitive function tasks. This limitation stems from the practical difficulties of utilizing positron emission tomography (PET) and magnetic resonance imaging (MRI) systems in hypoxic environments. We addressed these challenges by employing functional near-infrared spectroscopy (fNIRS), which requires only a compact experimental system, is portable, and can be readily installed in gym settings. Our findings revealed that exercise in hypoxic environments induces decreasing cognitive performance, specifically cognitive fatigue, by reducing task-specific neural activity. This chapter provides an overview of our research methodology and results.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"371-388"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Minimum Exercise Model in Humans Based on Oxygen Uptake and Physiological Parameters.","authors":"Morimasa Kato, Hyukki Chang, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_4","DOIUrl":"10.1007/978-981-95-0066-6_4","url":null,"abstract":"<p><p>Understanding exercise intensity is essential for optimizing training outcomes and minimizing health risks. This chapter introduces key physiological and subjective parameters used to assess exercise intensity, including heart rate reserve (HRR), oxygen uptake reserve (VO2R), maximal oxygen consumption (VO2max), and ratings of perceived exertion (RPE). Standardized classifications from organizations such as the American College of Sports Medicine (ACSM) are presented, alongside practical methods like the Talk Test for field applications. Incremental exercise testing is highlighted for identifying physiological thresholds, including lactate and ventilatory thresholds, which serve as critical markers for personalized training. Additionally, recent advances in neuroimaging-including electroencephalography (EEG), near-infrared spectroscopy (NIRS), and functional magnetic resonance imaging (fMRI)-are reviewed to explore how different exercise intensities affect brain activity. Evidence suggests that even low to moderate-intensity exercise can positively influence cognitive function and cerebral blood flow. The integration of wearable technologies has further enabled real-time monitoring of both physiological and neurocognitive responses. Overall, this chapter underscores the importance of individualized, evidence-based approaches in exercise prescription and highlights emerging methods for linking exercise intensity with brain function.</p>","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"83-93"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}