NeuroprotectionPub Date : 2019-04-03DOI: 10.5772/INTECHOPEN.81951
L. Mititelu-Tarțău, M. Bogdan, V. Gheorman, L. Foia, Ancuța Goriuc, G. Rusu, B. R. Buca, L. Pavel, A. Cristofor, C. Tartau, G. Popa
{"title":"Current Therapeutic Approaches from Imidazoline and Opioid Receptors Modulators in Neuroprotection","authors":"L. Mititelu-Tarțău, M. Bogdan, V. Gheorman, L. Foia, Ancuța Goriuc, G. Rusu, B. R. Buca, L. Pavel, A. Cristofor, C. Tartau, G. Popa","doi":"10.5772/INTECHOPEN.81951","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81951","url":null,"abstract":"Due to brain plasticity, the nervous system is capable of manifesting behavioral variations, adapted to the influences from both external and internal environment. Multiple neurotransmitters are involved in the mediation of pathological processes at the molecular, cellular, regional, and interregional levels participating in cerebral plasticity, their intervention being responsible for various structural, functional, and behavioral disturbances. The current therapeutic strategies in neuroprotection aim at blocking on different levels, the molecular cascades of the pathophysiological mechanisms responsible for neuronal dysfunctions and ultimately for neuronal death. Different agents influencing these neurotransmitters have demonstrated beneficial effects in neurogenesis and neuroprotection, proved in experimental animal models of focal and global ischemic injuries. Serotonin, dopamine, glutamate, N-methyl-D-aspartate, and nitric oxide have been shown to play a significant role in modulating nervous system injuries. The imidazoline system is one of the important systems involved in human brain functioning. Experimental investigations have revealed the cytoprotective effects of imidazoline I2 receptor ligands against neuronal injury induced by hypoxia in experimental animals. The neuroprotective effects were also highlighted for kappa and delta receptors, whose agonists demonstrated the ability to reduce architectural lesions and to recover neuronal functions of animals with experimentally induced brain ischemia.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87002104","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}
NeuroprotectionPub Date : 2019-03-27DOI: 10.5772/INTECHOPEN.85631
R. Chang, Y. Ho
{"title":"Introductory Chapter: Concept of Neuroprotection - A New Perspective","authors":"R. Chang, Y. Ho","doi":"10.5772/INTECHOPEN.85631","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.85631","url":null,"abstract":"","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88211288","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}
NeuroprotectionPub Date : 2019-03-07DOI: 10.5772/INTECHOPEN.84272
W. Aryati, Nabilah Nurtika Salamah, Rezi Riadhi Syahdi, Arry Yanuar
{"title":"The Role and Development of the Antagonist of Adenosine A2A in Parkinson’s Disease","authors":"W. Aryati, Nabilah Nurtika Salamah, Rezi Riadhi Syahdi, Arry Yanuar","doi":"10.5772/INTECHOPEN.84272","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.84272","url":null,"abstract":"Adenosine is a neuromodulator that regulates the body’s response to dopamine and another neurotransmitter in the brain that is responsible for motoric, emotion, learning, and memory function. Adenosine is a G-protein-coupled receptor and has four subtypes, which are A 1, A 2A , A 2B , and A 3 . Adenosine A 2A is located in the striatum of the brain. Antagonist interferes with GABA releasing, modulates acetyl-choline and releases dopamine, and also facilitates dopamine receptor’s signaling. Therefore, it can reduce motoric symptoms in Parkinson’s disease. Adenosine A 2A antagonist is also believed to have neuroprotective effects. Several compounds have been reported and have undergone clinical test as selective adenosine A 2A antagonists, including istradefylline, preladenant, tozadenant, vipadenant, ST-1535, and SYN-115. Nonselective adenosine A 2A antagonists from natural compounds are caffeine and theophylline. ,","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72890883","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}
NeuroprotectionPub Date : 2019-01-06DOI: 10.5772/INTECHOPEN.82330
S. Nian, A. Lo
{"title":"Protecting the Aging Retina","authors":"S. Nian, A. Lo","doi":"10.5772/INTECHOPEN.82330","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.82330","url":null,"abstract":"Aging retina, notably the aging macula, is prone to develop degenerative diseases, such as age-related macular degeneration (AMD), the leading cause of visual loss in individuals aged 65 or above in developed countries. However, current treatments are very limited. Since degeneration, dysfunction, and death of retinal neurons are demonstrated in the pathogenesis of AMD, neuroprotective strategies could serve as a possible way to treat AMD. In this chapter, we will briefly introduce risk factors, pathophysiology, affected neurons, classification, clinical manifestation, and current treatments of AMD. Finally, neuroprotection in both AMD animal models and patients will be discussed.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"253 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78381217","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}
NeuroprotectionPub Date : 2018-11-26DOI: 10.5772/INTECHOPEN.81343
Monika Sharma, Patrick Flood
{"title":"Adrenergic Receptors as Pharmacological Targets for Neuroinflammation and Neurodegeneration in Parkinson’s Disease","authors":"Monika Sharma, Patrick Flood","doi":"10.5772/INTECHOPEN.81343","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81343","url":null,"abstract":"Inflammation is a key component of the dopaminergic neurodegeneration seen in progressive Parkinson’s disease (PD). The presence of activated glial cells, the participation of innate immune system, increased inflammatory molecules such as cytokines and chemokines, and increased oxidative stress and reactive oxygen species are the main neuroinflammatory characteristics present in progressive PD. Therapeutic targets which suppress pro-inflammatory responses by glial cells (mainly microglia) have been shown to be effective treatments for slowing or eliminating the progressive degeneration of neurons within the substantia nigra. In this chapter, we will detail a specific anti-inflammatory therapy using agonists to β 2-adrenergic receptors that have been shown to be effective treatments for models of dopaminergic neurodegeneration and that have had efficacy in patients with progressive PD. We will also detail the possible molecular mechanisms of action of this therapeutic in stopping or reversing inflammation within the CNS.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87289399","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}
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