神经保护
神经再生
创伤性脑损伤
六烯酸
脊髓损伤
医学
多不饱和脂肪酸
二十碳五烯酸
神经可塑性
药理学
脊髓
精神科
脂肪酸
生物
生物化学
作者
Adina T. Michael‐Titus,John V. Priestley
标识
DOI:10.1016/j.tins.2013.10.005
摘要
•Evidence for positive effects of omega-3 polyunsaturated fatty acids (PUFA) in CNS. •Omega-3 PUFAs potential treatment for spinal cord or traumatic brain injury. •Omega-3 PUFA delivery after or dietary exposure prior to injury improves outcomes. •Neuroprotective effects of omega-3 PUFAs likely mediated via multiple pathways. •Understanding role of omega-3 PUFAs in neuroplasticity critical next step. Omega-3 polyunsaturated fatty acids (PUFAs) are compounds that have a structural role in the nervous system and are essential for neurodevelopment. Results obtained with docosahexaenoic acid and eicosapentaenoic acid show therapeutic potential in neurotrauma. Traumatic brain injury (TBI) and spinal cord injury (SCI) can lead to major disability and have a significant socioeconomic cost. Thus, there is an unmet need for acute neuroprotection and for treatments that promote neuroregeneration. Acute administration of omega-3 PUFAs after injury and dietary exposure before or after injury improve neurological outcomes in experimental SCI and TBI. The mechanisms involved include decreased neuroinflammation and oxidative stress, neurotrophic support, and activation of cell survival pathways. This review raises questions that must be addressed before successful clinical translation. Omega-3 polyunsaturated fatty acids (PUFAs) are compounds that have a structural role in the nervous system and are essential for neurodevelopment. Results obtained with docosahexaenoic acid and eicosapentaenoic acid show therapeutic potential in neurotrauma. Traumatic brain injury (TBI) and spinal cord injury (SCI) can lead to major disability and have a significant socioeconomic cost. Thus, there is an unmet need for acute neuroprotection and for treatments that promote neuroregeneration. Acute administration of omega-3 PUFAs after injury and dietary exposure before or after injury improve neurological outcomes in experimental SCI and TBI. The mechanisms involved include decreased neuroinflammation and oxidative stress, neurotrophic support, and activation of cell survival pathways. This review raises questions that must be addressed before successful clinical translation.
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