Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches最新文献

Amyotrophic Lateral Sclerosis 肌萎缩侧索硬化症

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2021-01-20 DOI: 10.5772/intechopen.92724

Robin Warner

引用次数: 1

Cerebellum: Its Anatomy, Functions and Diseases 小脑:解剖、功能和疾病

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2020-06-24 DOI: 10.5772/INTECHOPEN.93064

Rajani Singh

{"title":"Cerebellum: Its Anatomy, Functions and Diseases","authors":"Rajani Singh","doi":"10.5772/INTECHOPEN.93064","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.93064","url":null,"abstract":"Cerebellum is the largest part of the hindbrain and weighs about 150 g. It is enshrined in posterior cranial fossa behind the pons and medulla oblongata and separated from these structures by cavity of fourth ventricle. It is connected to brainstem by three fibre tracts known as cerebellar peduncles. Cerebellum controls the same side of body. It precisely coordinates skilled voluntary movements by controlling strength, duration and force of contraction, so that they are smooth, balanced and accurate. It is also responsible for maintaining equilibrium, muscle tone and posture of the body. This is achieved through the use of somatic sensory information in modulating the motor output from the cerebrum and brainstem. Sherrington regarded cerebellum as the head ganglion of the proprioceptive system. Dysfunction of cerebellum along with degenerative diseases of cerebellum such as spinocerebellar ataxia, multiple sclerosis, malignant tumours, etc. may culminate into disequilibrium, hypotonia, difficulty in talking, sleeping, maintaining muscular coordination and dyssynergia which at times may be life threatening. Hence, knowledge of anatomy of cerebellum is imperative for neuroanatomists and neurosurgeons.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"2011 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114703845","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: 5

Molecular Mechanisms behind Initiation of Focal Seizure in Temporal Lobe Epilepsy: Computational Study 颞叶癫痫局灶性发作起始的分子机制:计算研究

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2020-06-19 DOI: 10.5772/intechopen.92846

Ruchi Jakhmola Mani, D. Katare

{"title":"Molecular Mechanisms behind Initiation of Focal Seizure in Temporal Lobe Epilepsy: Computational Study","authors":"Ruchi Jakhmola Mani, D. Katare","doi":"10.5772/intechopen.92846","DOIUrl":"https://doi.org/10.5772/intechopen.92846","url":null,"abstract":"Epilepsy is a noncommunicable disease of the brain that affects people of all ages. The chapter aims to identify protein targets and their mechanism of action behind temporal lobe epilepsy. Differentially expressed proteins in temporal lobe epilepsy (TLE) were used to derive a hypothesis demonstrating routes of protein interactions causing focal seizure and identification of putative target receptor for its treatment. Text mining was done by constructing a Boolean query with keywords such as temporal lobe epilepsy, focal seizures, proteomics, etc., in different scientific search engines. The proteins were further used for creating protein interaction network and analysed for their role in focal epileptic seizure pathway. The most appropriate route for initiation of seizure was observed to be route 3. It describes the dysregulated signal transduction from adenosine A1 receptor (ADORA1) to gamma-aminobutyric acid (GABA) B receptor 1 (GABBR1). This causes electrical imbalance and hyper-excitation of neurons that lead to focal seizure. The study also predicts that YWHAZ (3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta) could be the potential target for preventing focal seizures. The network framed in this study is ideal for studying the cascades of events that may occur during focal seizures in TLE and is useful in drug discovery.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132546897","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: 1

The Brain Stress System in the Neurobiology of the “Dark Side” of Addiction and Its Relation to Neurodegeneration 成瘾“阴暗面”的神经生物学中的脑应激系统及其与神经变性的关系

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2020-06-01 DOI: 10.5772/intechopen.93152

Maria Uscinska, Nicolo’ Gagliano, F. H. Lai

{"title":"The Brain Stress System in the Neurobiology of the “Dark Side” of Addiction and Its Relation to Neurodegeneration","authors":"Maria Uscinska, Nicolo’ Gagliano, F. H. Lai","doi":"10.5772/intechopen.93152","DOIUrl":"https://doi.org/10.5772/intechopen.93152","url":null,"abstract":"Addiction is a chronically relapsing disorder characterized by a compulsion to seek and take a substance of abuse, the development of dependence, and a negative emotional state when intake is stopped. Compelling evidence argues that dysregulation of the brain stress system is a key constituent of the addiction process. Through mechanisms of negative reinforcement, the stress system is posited to induce negative emotional state referred to as the ‘dark side of addiction’ as it becomes the powerful motivation for drug-seeking associated with compulsive use. Therein, the neuropharmacological actions of corticotropin-releasing factor (CRF) is posited to play a key role in the anxiety/stress-like effects of acute withdrawal, anxiety/stress-like effects of abstinence, and relapse to drug taking. In this view, the present chapter sheds a critical light on latest research developments implicating this largely neglected component of substance abuse to give insight into the neuropathology of the ‘dark side’ of addiction. Moreover, the chapter provides insight into individual vulnerability to addiction and proposes a novel treatment candidate for the disorder.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131278748","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: 2

Alzheimer’s Disease and Type 2 Diabetes Mellitus: Molecular Mechanisms and Similarities 阿尔茨海默病和2型糖尿病:分子机制和相似性

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2020-05-21 DOI: 10.5772/intechopen.92581

K. I. L. León, A.D. Bertadillo-Jilote, D. García-Gutiérrez, M. Meraz-Ríos

{"title":"Alzheimer’s Disease and Type 2 Diabetes Mellitus: Molecular Mechanisms and Similarities","authors":"K. I. L. León, A.D. Bertadillo-Jilote, D. García-Gutiérrez, M. Meraz-Ríos","doi":"10.5772/intechopen.92581","DOIUrl":"https://doi.org/10.5772/intechopen.92581","url":null,"abstract":"Alzheimer’s disease (AD) has become one of the most threatening diseases in the elderly, and type 2 diabetes mellitus (T2DM) is a major health problem in the world, representing 7.4% of the population. Several studies have produced epidemiological, clinical, and pathological evidence of the relationship between AD and T2DM. Laboratory research using animal models has identified mechanisms shared by both T2DM and AD. Particularly, there is an increase of tau phosphorylation and cleavage, which is known to be particularly toxic to neurons and to form a nucleation for neurofibrillary tangles. Also, alterations in synaptic plasticity are associated to tau pathology through the direct abnormal interaction of pathological tau with synaptic proteins and indirectly through Tau-activated neuroinflammatory processes. Many T2DM complications are potentiated or initiated by the accumulation of specific forms of advanced glycation end products (AGEs) and their interaction with its receptors (RAGE). AGEs promote β-amyloid aggregation and cytotoxicity, while glycation of tau may enhance their aggregation. Therefore, this review addresses the analysis of the common mechanisms where the major molecular players of these two diseases participate and contribute to a better understanding of these diseases in their pathogenic relationship.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131706650","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: 3

Brain-Derived Neurotrophic Factor and Stem Cell-Based Technologies in Huntington’s Disease Therapy 脑源性神经营养因子和干细胞技术在亨廷顿病治疗中的应用

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2020-02-19 DOI: 10.5772/intechopen.91226

I. Kerkis, Joyce Macedo da Silva, C. Wenceslau, N. C. Mambelli-Lisboa, E. Frare

{"title":"Brain-Derived Neurotrophic Factor and Stem Cell-Based Technologies in Huntington’s Disease Therapy","authors":"I. Kerkis, Joyce Macedo da Silva, C. Wenceslau, N. C. Mambelli-Lisboa, E. Frare","doi":"10.5772/intechopen.91226","DOIUrl":"https://doi.org/10.5772/intechopen.91226","url":null,"abstract":"Neurodegenerative disorders, such as Huntington’s disease (HD), Alzheimer’s disease (AD), and Parkinson’s disease (PD), are characterized by changes in the levels and activities of neurotrophic factors (NTFs), such as brain-derived neurotrophic factor (BDNF). Gain-of-function and loss-of-function experiments demonstrate in fact the linkage between wild-type huntingtin (HTT) and gene transcription and intracellular transport of BDNF. In the present chapter, we will analyze the involvement of BDNF in HD and other neurodegenerative diseases. We will discuss the current BDNF technologies focusing on stem cell therapies that induce BDNF upregulation, for instance, the method of autologous mesenchymal stem cell (MSC) culturing in the presence of cocktail of BDNF inducers and factors (MSC/BDNF), genetic engineering of MSC and their use as a vector for BDNF gene delivery, and combined method of establishment of embryonic stem cell (ESC)-derived BDNF-overexpressing neural progenitors, which is still at the preclinical stage. Clinical trial that uses MSC/BDNF is already in course, while genetic engineering of MSC/BDNF is in perspective to treat adult and juvenile HD. The potential application of these technologies is beyond HD. Other neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases also can be further included in the list of clinical trials that use MSC/BDNF or even ESC/BDNF-overexpressing neural progenitors.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123895230","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: 3

Electrophysiological Investigations of Prion Protein Roles in Health and Disease 朊蛋白在健康和疾病中的作用的电生理研究

Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches Pub Date : 2019-11-08 DOI: 10.5772/intechopen.90049

S. Foliaki, B. Groveman, C. Haigh

{"title":"Electrophysiological Investigations of Prion Protein Roles in Health and Disease","authors":"S. Foliaki, B. Groveman, C. Haigh","doi":"10.5772/intechopen.90049","DOIUrl":"https://doi.org/10.5772/intechopen.90049","url":null,"abstract":"Prion diseases are transmissible and fatal neurological disorders associated with the misfolding of cellular prion protein (PrPC) into disease-causing isoforms (PrPD) in the central nervous system. The diseases have three etiologies; acquired through exposure to the infectious PrPD, sporadic, arising from no known cause, and hereditary due to familial mutations within the PRNP gene. The manifestation of clinical signs is associated with the disruption of neuronal activity and subsequent degeneration of neurons. To generate insight into the mechanisms by which neuronal activity becomes disrupted in prion diseases, electrophysiological techniques have been applied to closely study the electrical signaling properties of neurons that lack functional PrPC as well as neurons that are developing pathological features of prion diseases due to infection or genetic mutation. In this review, we will compile the electrophysiological evidences of neurophysiological roles of PrPC, how those roles are changed in neurons that are developing prion diseases, and how disease-associated effects are exacerbated during the clinical stage of disease.","PeriodicalId":302815,"journal":{"name":"Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127679692","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: 1