Pub Date : 2019-10-10DOI: 10.5772/intechopen.89539
Roxana Rodríguez-Barrera, Marcela Garibay-López, A. Ibarra
Spinal cord injury (SCI) is an important pathology leading to possibly fatal consequences. The most common repercussions are those affecting motor and sensitivity skills. SCI-damage occurs in its first phase—as a result of the lesion mechanism (contusion, compression, transection, and primary lesion). After this primary damage, there is a second phase with further deleterious effects on neural degeneration and tissue restoration. At the moment, several investigation groups are working on developing therapeutic strategies to induce neuroprotection. This chapter pretends to introduce the reader to a wide range of these therapies, particularly those with promising results and tested in preclinical and clinical studies. In the first section, physiopathology of SCI will be addressed. Afterwards, the chapter will review neuroprotective strategies such as cyclooxygenase, calpain, and apoptosis inhibitors. Finally, the effect of immunophilin ligands, neural-derived peptides, antioxidants, hypoglycemic agent, gonadal hormones, Na channel blockers, and transplant of cultured cells will also be reviewed.
{"title":"Trends in Neuroprotective Strategies after Spinal Cord Injury: State of the Art","authors":"Roxana Rodríguez-Barrera, Marcela Garibay-López, A. Ibarra","doi":"10.5772/intechopen.89539","DOIUrl":"https://doi.org/10.5772/intechopen.89539","url":null,"abstract":"Spinal cord injury (SCI) is an important pathology leading to possibly fatal consequences. The most common repercussions are those affecting motor and sensitivity skills. SCI-damage occurs in its first phase—as a result of the lesion mechanism (contusion, compression, transection, and primary lesion). After this primary damage, there is a second phase with further deleterious effects on neural degeneration and tissue restoration. At the moment, several investigation groups are working on developing therapeutic strategies to induce neuroprotection. This chapter pretends to introduce the reader to a wide range of these therapies, particularly those with promising results and tested in preclinical and clinical studies. In the first section, physiopathology of SCI will be addressed. Afterwards, the chapter will review neuroprotective strategies such as cyclooxygenase, calpain, and apoptosis inhibitors. Finally, the effect of immunophilin ligands, neural-derived peptides, antioxidants, hypoglycemic agent, gonadal hormones, Na channel blockers, and transplant of cultured cells will also be reviewed.","PeriodicalId":165931,"journal":{"name":"Neuroprotection - New Approaches and Prospects","volume":"13 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133036716","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}
Pub Date : 2019-09-19DOI: 10.5772/intechopen.89416
Katheryn Broman, Abigail U. Davis, J. May, Han-A Park
The brain requires vast amounts of energy to carry out neurotransmission; indeed, it is responsible for approximately one-fifth of the body’s energy consumption. Therefore, in order to understand functions of brain cells under both normal and pathological conditions, it is critical to elucidate dynamics of intracellular energy. The mitochondrion is the key intercellular organelle that controls neuronal energy and survival. Numerous studies have reported a correlation between altered mitochondrial function and brain-associated diseases; thus mitochondria may serve as a promising target for treating these conditions. In this chapter, we will discuss the mechanisms of mitochondrial production, movement, and degradation in order to understand accessibility of energy during physiological and pathological conditions of the brain. While research targeting molecular dynamics is promising, translation into clinical relevance based on bench research is challenging. For these reasons, we will also summarize lifestyle factors, including interventions and chronic comorbidities that disrupt mitochondrial dynamics. By determining lifestyle factors that are readily accessible, we can propose a new viewpoint for a synergistic and translational approach for neuroprotection.
{"title":"Lifestyle Factors, Mitochondrial Dynamics, and Neuroprotection","authors":"Katheryn Broman, Abigail U. Davis, J. May, Han-A Park","doi":"10.5772/intechopen.89416","DOIUrl":"https://doi.org/10.5772/intechopen.89416","url":null,"abstract":"The brain requires vast amounts of energy to carry out neurotransmission; indeed, it is responsible for approximately one-fifth of the body’s energy consumption. Therefore, in order to understand functions of brain cells under both normal and pathological conditions, it is critical to elucidate dynamics of intracellular energy. The mitochondrion is the key intercellular organelle that controls neuronal energy and survival. Numerous studies have reported a correlation between altered mitochondrial function and brain-associated diseases; thus mitochondria may serve as a promising target for treating these conditions. In this chapter, we will discuss the mechanisms of mitochondrial production, movement, and degradation in order to understand accessibility of energy during physiological and pathological conditions of the brain. While research targeting molecular dynamics is promising, translation into clinical relevance based on bench research is challenging. For these reasons, we will also summarize lifestyle factors, including interventions and chronic comorbidities that disrupt mitochondrial dynamics. By determining lifestyle factors that are readily accessible, we can propose a new viewpoint for a synergistic and translational approach for neuroprotection.","PeriodicalId":165931,"journal":{"name":"Neuroprotection - New Approaches and Prospects","volume":"104 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122669980","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}
Pub Date : 2019-09-09DOI: 10.5772/intechopen.88974
O. Klementieva
Finding successful therapies for the treatment of Alzheimer’s disease (AD) is one of the most challenging tasks existing for human health. Several drugs have been found and validated in preclinical studies with some success, but not with the desired breakthroughs in the following clinical development phases. AD causes multiple brain dysfunctions that can be described as a brain organ failure, resulting in significant cognitive decline. Aggregation of amyloid proteins and neuronal loss are the hallmarks of AD. Thus, one of the strategies to treat AD is to find a multifunctional drug that may combine both anti-aggregation and neuroprotective properties. Such a candidate could be chemically modified dendrimers. Dendrimers are branched, nonlinear molecules with multiple reactive groups located on their surface. Chemical modification of reactive surface groups defines the property of the dendrimers. In this chapter, I will discuss poly(propylene imine) dendrimers with the surface functionalized with histidine and maltose as an example of a multifunctional therapeutic drug candidate able to protect the memory of AD transgenic model mice.
{"title":"Glycodendrimers as Potential Multitalented Therapeutics in Alzheimer’s Disease","authors":"O. Klementieva","doi":"10.5772/intechopen.88974","DOIUrl":"https://doi.org/10.5772/intechopen.88974","url":null,"abstract":"Finding successful therapies for the treatment of Alzheimer’s disease (AD) is one of the most challenging tasks existing for human health. Several drugs have been found and validated in preclinical studies with some success, but not with the desired breakthroughs in the following clinical development phases. AD causes multiple brain dysfunctions that can be described as a brain organ failure, resulting in significant cognitive decline. Aggregation of amyloid proteins and neuronal loss are the hallmarks of AD. Thus, one of the strategies to treat AD is to find a multifunctional drug that may combine both anti-aggregation and neuroprotective properties. Such a candidate could be chemically modified dendrimers. Dendrimers are branched, nonlinear molecules with multiple reactive groups located on their surface. Chemical modification of reactive surface groups defines the property of the dendrimers. In this chapter, I will discuss poly(propylene imine) dendrimers with the surface functionalized with histidine and maltose as an example of a multifunctional therapeutic drug candidate able to protect the memory of AD transgenic model mice.","PeriodicalId":165931,"journal":{"name":"Neuroprotection - New Approaches and Prospects","volume":"42 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129673908","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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