Advances in neurobiology最新文献_第5页

Exercise as a Therapeutic Intervention for Alzheimer's Disease. 运动作为阿尔茨海默病的治疗干预。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-981-95-0066-6_16

Dong-Joo Hwang, Joon-Yong Cho

{"title":"Exercise as a Therapeutic Intervention for Alzheimer's Disease.","authors":"Dong-Joo Hwang, Joon-Yong Cho","doi":"10.1007/978-981-95-0066-6_16","DOIUrl":"10.1007/978-981-95-0066-6_16","url":null,"abstract":"Alzheimer's disease (AD) is a common form of dementia characterized by cognitive decline and abnormal accumulation of proximate neurotoxins in older adults. It accounts for up to 80% of all dementia cases. AD is not exclusively attributed to aging; rather, it involves complex and multifactorial brain changes that can lead to severe functional dependence and ultimately death. Although there has been progress in the development of novel treatments for AD, they are yet to yield disease-modifying effects. Early detection and therapeutic interventions are critical for preventing or delaying the onset of AD. We aimed to provide an overview of emerging evidence on physical exercise as a therapeutic strategy for the prevention and treatment of AD. Studies have demonstrated the potential of exercise in improving cognitive function, reducing the risk of AD, and slowing disease progression by promoting various neuroplastic changes. Therefore, regular exercise should be considered as a disease-modifying intervention for AD and included in comprehensive treatment protocols. Further studies are warranted to establish the optimal exercise regimen for individuals with AD; nonetheless, incorporating exercise into daily routines may contribute toward the prevention and management of AD.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"297-316"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147366","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}

引用次数: 0

Novel Ways of Targeting the Dopamine Transporter. 靶向多巴胺转运体的新方法。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-96364-3_11

Yibin Xu, Hanming Zeng, Shaili Aggarwal, Ole Valente Mortensen

{"title":"Novel Ways of Targeting the Dopamine Transporter.","authors":"Yibin Xu, Hanming Zeng, Shaili Aggarwal, Ole Valente Mortensen","doi":"10.1007/978-3-031-96364-3_11","DOIUrl":"10.1007/978-3-031-96364-3_11","url":null,"abstract":"Dopamine (DA) is an important modulatory neurotransmitter that is involved in daily activities such as movement, memory, and reward-oriented learning of essential behaviors and needs. DA signaling is initiated by the release of DA into the synaptic cleft that will bind to dopamine receptors to mediate the physiological response. To terminate the DA response, the DA is taken up by the dopamine transporter (DAT), a surface membrane protein. Psychostimulants, like cocaine and amphetamine, both target DAT and interfere with the DA uptake process, resulting in an increased amount of DA in the synaptic cleft. Continuous use of psychostimulants can lead to psychostimulant use disorders (PUDs), which are marked by uncontrollable psychostimulant craving and misuse. Because of the unmet need for treatment options for PUDs, novel strategies for discovering therapies are essential. Over the years, DAT-targeting ligands have been identified with atypical properties such as reduced abuse liability compared to cocaine. These compounds have been proposed to bind to different sites from cocaine and/or prefer and stabilize specific conformations of DAT. In addition, some of these compounds can interfere with psychostimulant-DAT binding and may have therapeutic potential in treating PUDs. This chapter introduces the role of DAT in PUDs, presents the mechanism of action of novel DAT-binding ligands, and discusses the therapeutic potential of atypical DAT-binding ligands for PUDs.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"46 ","pages":"271-292"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12604107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuroglial Pathophysiology of Leukodystrophies. 脑白质营养不良的神经胶质病理生理学。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-87919-7_10

Alexei Verkhratsky, Jianqin Niu, Chenju Yi, Arthur Butt

{"title":"Neuroglial Pathophysiology of Leukodystrophies.","authors":"Alexei Verkhratsky, Jianqin Niu, Chenju Yi, Arthur Butt","doi":"10.1007/978-3-031-87919-7_10","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_10","url":null,"abstract":"Leukodystrophies are a diverse group of inherited diseases characterised by white matter degenerative pathology. Leukodystrophies have a highly heterogeneous genetic background linked mainly to mutations in oligodendrocyte and astrocyte genes and, to lesser extent, microglia. The most prevalent leukodystrophies are caused by mutations in oligodendrocyte genes that encode the essential myelin proteins PLP1 and GalC in Pelizaeus-Merzbacher disease and Krabbe disease, respectively. Astrocyte leukodystrophies are led by Alexander disease, caused by mutations in the astrocyte gene GFAP. Vanishing white matter disease, the most prevalent inherited white matter pathology in children, is associated with astrocyte atrophy and cystic degeneration of the cerebral white matter. The pathogenic mechanisms in leukodystrophies depend on the genetic mutations and hence are extremely varied, but the diseases have in common white matter atrophy caused by the loss of oligodendrocytes and myelin, with or without marked reactive astrogliosis and microglia activation. The development of a range of animal models with the disruption of specific genes causing leukodystrophies and the use of pluripotent stem cells from people with different forms of leukodystrophy is advancing the understanding of the functional and cellular pathophysiology of these rare diseases.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"257-279"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273958","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}

引用次数: 0

Plasticity of Myelination. 髓鞘形成的可塑性。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-87919-7_8

Grace Flower, Svenja Vorthmann, Daniel Fulton, Nicola B Hamilton

{"title":"Plasticity of Myelination.","authors":"Grace Flower, Svenja Vorthmann, Daniel Fulton, Nicola B Hamilton","doi":"10.1007/978-3-031-87919-7_8","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_8","url":null,"abstract":"Myelin plasticity, the capacity for dynamic changes in myelination and myelin structure, challenges the long-held view of myelin as a static entity post-development. Emerging evidence highlights its pivotal role in adapting neural circuits during learning, memory, and recovery from injury or disease. This chapter explores the cellular and molecular mechanisms underlying myelin plasticity, focusing on activity-dependent and experience-driven myelination mediated by oligodendrocytes, which are potentially modified by astrocytes and microglia. This study examines how neuronal activity regulates oligodendrocyte differentiation and myelin remodelling, affecting conduction velocity and circuit synchronization. The implications of myelin plasticity in cognition, ageing, and pathologies such as multiple sclerosis and stroke are discussed alongside experimental models that elucidate its processes. Finally, the importance of sleep in myelin maintenance and plasticity is discussed. Elucidating the mechanisms underlying myelin plasticity and maintenance may uncover new therapeutic opportunities for treating diseases and injuries that disrupt myelin and neuronal activity.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"181-204"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273964","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}

引用次数: 0

Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases. 神经退行性疾病中少突胶质细胞的蛋白质病理。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-87919-7_14

Shelley L Forrest, Gabor G Kovacs

{"title":"Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases.","authors":"Shelley L Forrest, Gabor G Kovacs","doi":"10.1007/978-3-031-87919-7_14","DOIUrl":"https://doi.org/10.1007/978-3-031-87919-7_14","url":null,"abstract":"Neurodegenerative diseases are clinically, pathologically and genetically heterogeneous disorders characterised by progressive dysfunction and neuronal loss and the deposition of disease-specific proteinaceous aggregates in neurons and/or glia, showing a hierarchical involvement of brain regions. Research into disease mechanisms underlying neurodegenerative disorders has focused on the proteinaceous neuronal aggregates in vulnerable brain regions leading to neuronal dysfunction and degeneration and onset of clinical symptoms. However, emerging evidence highlights the importance of glia, including oligodendroglia, in the pathogenesis of neurodegenerative diseases, which have been underappreciated and frequently considered secondary to neuronal involvement. Pathologically altered proteins depositing in oligodendroglia comprise phosphorylated tau, α-synuclein, transactive response DNA-binding protein-43 (TDP-43) and occasionally FET/FUS. However, only primary oligodendroglial tau and α-synuclein deposits are considered for neuropathological diagnosis and classification of some tauopathies and synucleinopathies, respectively. Oligodendroglial tau pathology is also seen in ageing-related tau oligodendrogliopathy (ARTOG). This chapter provides an overview of neurodegenerative proteinopathies and protein pathologies affecting oligodendroglia.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"43 ","pages":"407-432"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144273965","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}

引用次数: 0

Physiology of Oligodendroglia. 少突胶质细胞生理学。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-87919-7_6

Arthur Butt, Adam Willis, Ian Hunter, Jianqin Niu, Chenju Yi, Alexei Verkhratsky

引用次数: 0

Neuronal Activity in Rat Hippocampus During Light-Intensity Treadmill Running. 轻强度跑步机运动大鼠海马神经元活动。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-981-95-0066-6_2

Takeshi Nishijima, Hideaki Soya

{"title":"Neuronal Activity in Rat Hippocampus During Light-Intensity Treadmill Running.","authors":"Takeshi Nishijima, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_2","DOIUrl":"10.1007/978-981-95-0066-6_2","url":null,"abstract":"In the early 2000s, it became evident that exercise enhances brain function, particularly in the hippocampus, attracting considerable attention. However, at that time, most studies relied on the voluntary wheel running model for experiments, it was unclear whether exercise conditions affected the impact of exercise on the hippocampus. Therefore, aiming to obtain translational insights applicable to humans, we focused on exercise intensity and started with the research investigating whether light-intensity exercise activates hippocampal neural activity in rats. We established an original running model in rats comprising laser Doppler flowmetry for monitoring hippocampal cerebral blood flow (Hip-CBF) and microdialysis for drug treatment. We found that Hip-CBF increased with light-intensity treadmill running, which was elicited by hippocampal neuronal activation and subsequent N-methyl-D-aspartate/nitric oxide (NMDA/NO) signaling. In this chapter, we first retrospectively summarize what we knew and what we did not know during that time, and the impact of our findings that light-intensity exercise can evoke neuronal activity in the rat hippocampus on our subsequent research.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147446","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}

引用次数: 0

Treadmill Running Model for Rodents as a Translational Approach Based on Human Physiological Responses. 基于人类生理反应的啮齿动物跑步机模型的翻译方法。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-981-95-0066-6_1

Masahiro Okamoto, Toshiaki Hata, Taichi Hiraga, Hideaki Soya

{"title":"Treadmill Running Model for Rodents as a Translational Approach Based on Human Physiological Responses.","authors":"Masahiro Okamoto, Toshiaki Hata, Taichi Hiraga, Hideaki Soya","doi":"10.1007/978-981-95-0066-6_1","DOIUrl":"10.1007/978-981-95-0066-6_1","url":null,"abstract":"The concept of \"Exercise is Medicine\" highlights the preventive effects of physical activity on lifestyle-related diseases, dementia, and mental disorders. However, human studies face limitations in isolating exercise-specific effects due to uncontrolled variables such as diet and living conditions, as well as the constraint of non-invasive methodologies. Animal models offer a valuable alternative, allowing for strict control of experimental conditions and detailed assessment of physiological and neural responses to exercise. While voluntary wheel running has been commonly used, it lacks standardization in exercise intensity and type. To bridge this gap, we developed a treadmill-based rodent exercise model that enables precise control over exercise parameters, including intensity, duration, and distance. By incorporating physiological markers-such as blood lactate and oxygen consumption-commonly used in humans, we succeeded in evaluating rodent fitness and establishing exercise paradigms analogous to those used in human studies. Our findings demonstrate that even light-intensity exercise can significantly enhance brain activation and memory, which may be particularly relevant for aging or low-fitness populations. This approach enables the exploration of shared neurobiological mechanisms and supports the advancement of translational research, facilitating the development of tailored exercise interventions aimed at promoting cognitive health.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"44 ","pages":"3-19"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147480","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}

引用次数: 0

Monoamine-Uptake Inhibitors and Pain: Antidepressant Drugs Among First-Line Treatments Against Neuropathic Pain and Fibromyalgia. 单胺摄取抑制剂和疼痛：抗抑郁药物是神经性疼痛和纤维肌痛的一线治疗。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-96364-3_12

Michel Barrot, Henrico-Pio Basile, Mélanie Kremer

{"title":"Monoamine-Uptake Inhibitors and Pain: Antidepressant Drugs Among First-Line Treatments Against Neuropathic Pain and Fibromyalgia.","authors":"Michel Barrot, Henrico-Pio Basile, Mélanie Kremer","doi":"10.1007/978-3-031-96364-3_12","DOIUrl":"10.1007/978-3-031-96364-3_12","url":null,"abstract":"Some monoamine-uptake inhibitors are among first-line treatments for specific chronic pain conditions. It concerns tricyclic antidepressant drugs, such as amitriptyline or nortriptyline, and the more selective serotonergic and noradrenergic reuptake inhibitors, such as duloxetine. They are recommended for treating neuropathic pain, which is pain caused by a lesion or disease of the somatosensory nervous system, and fibromyalgia, which is a chronic widespread pain. Clinically, their action on pain was proposed to be independent from the one on depression. Research in animal models provided some understanding of the pain-relieving mechanism. The noradrenergic component of monoamine-uptake inhibitors appears to be critical, with the therapeutic effect likely involving targets at peripheral, spinal and supraspinal levels. At least two independent mechanisms would contribute to pain relief. One is spinal, relying on the recruitment of aminergic descending controls of pain, with a downstream key role of the α2 adrenergic receptors; the other may require more sustained treatment and relies on the noradrenergic recruitment of β2 adrenergic receptors and a downstream anti-neuroimmune action. Both mechanisms require a functional endogenous opioid system. These insights, however, focused on the sensory component of pain, and the contribution of the supraspinal action of antidepressant drugs needs to be explored in detail.","PeriodicalId":7360,"journal":{"name":"Advances in neurobiology","volume":"46 ","pages":"293-315"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145231294","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}

引用次数: 0

Regulation of Dopamine Transporter Surface Expression. 多巴胺转运体表面表达的调控。

Advances in neurobiology Pub Date : 2025-01-01 DOI: 10.1007/978-3-031-96364-3_4

Christina Besada, Ole Valente Mortensen

引用次数: 0