Neuroprotective effects of the survival promoting peptide Y-P30
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Brain and spinal cord (CNS) trauma typically directly kill some neurons leading to permanent neurological deficits. However, they also lead to a number of triggers which in turn frequently kill a vastly larger number of neurons than were killed by the initial insult. The best mechanism for reducing the extent of neurological deficits is to minimize the number of neurons that die immediately due to the trauma, and post-trauma sequelae. Neuroprotection techniques have taken many diverse forms with a breadth too great for a short review. Therefore, this review is focused on the roles of only a small number of neuroprotective agents, with its primary focus being on neuroprotection provided by hypothermia, alone and when combined with the other methods. Included are also recent results involving a novel neuroprotective technique, tested on adult human dorsal root ganglion neurons, comparing the influences of hypothermia and alkalinization singly, providing fourfold and eightfold increases in neuroprotection, respectively, but when combined providing a 26-fold increase in neuroprotection. This combinatorial approach to neuroprotection holds great promise for enhancing the degree of neuroprotection clinically following CNS trauma, leading to the preservation of maximal neurological functions.
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Brain and spinal cord (CNS) trauma typically kill a number of neurons, but even more neurons are killed by secondary causes triggered by the initial trauma. Thus, a minor insult may rapidly cause the death of a vastly larger number of neurons and complete paralysis. The best mechanism for reducing the extent of neurological deficits is to minimize the number of neurons killed by post‐trauma sequelae. Neuroprotection techniques take many diverse forms with a breadth too great for a short review. Therefore, this review focuses on the neuroprotection provided by hypothermia and a number of other neuroprotective techniques, when administered singly or in combination, because it is generally found that combinations of applications lead to significantly better neuroprotection than is achieved by any one alone. The combinatorial approach to neuroprotection holds great promise for enhancing the degree of neuroprotection following trauma, leading to maximum maintenance of neurological function.
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Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
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Herbal bioactive compounds have been investigated to possess neuroprotective properties. They are involved in the modulation of different signaling pathways that may facilitate neuroprotection. In this brief review, some of the promising compounds and their potential neuroprotective effects have been reported. They can be potential sources of therapeutics for neurodegenerative disorders.
KEYWORDS: neuroprotective, herbal, bioactive compounds, neurodegenerative diseases
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Neuroprotective agents aim to prevent neuronal death by inhibiting one or more of the pathophysiological steps in the processes that follow brain injury or ischemia due to occlusion of a cerebral artery. They also protect against neurodegeneration and neurotoxins. Application of new molecular technologies to dissect pathways and unravel mechanisms involved in damage to the nervous system are providing bases for development of new neuroprotective agents for diseases, which are currently treated by drugs that merely provide symptomatic relief. The topic is described in detail in the Handbook of Neuroprotection (Jain 2011). The concept of neuroprotection is now incorporated in development of drugs for neurologic disorders and more than 500 such approaches are in development including several that are based on biotechnology. For developing new neuroprotective strategies, it is important to understand the intrinsic neuroprotective factors in the human body.
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Neuroprotective agents are medications that can alter the course of metabolic events and have neuroprotective function. Neuroprotective agents are needed in patients undergoing a surgical procedure and clinical conditions that correspond with the central nervous system (CNS); also, in intensive care, the neuroprotective agents are often used to prevent complications and patient deterioration. Over the years, there is still no clear understanding of the potential for neuroprotection and the interactions between various drugs that serve a crucial role in anesthetic care and critical illness. This literature review will discuss further the mechanism of neuronal damage and various neuroprotective agents.
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