Therapeutic implications of how TNF links apolipoprotein E, phosphorylated tau, α-synuclein, amyloid-β and insulin resistance in neurodegenerative diseases.
Therapeutic implications of how TNF links apolipoprotein E, phosphorylated tau, α-synuclein, amyloid-β and insulin resistance in neurodegenerative diseases.
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DOI：
10.1111/bph.14471
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发表时间：
2018-10
影响因子：
7.3
通讯作者：
Vissel B
中科院分区：
文献类型：
--
作者：
Clark IA;Vissel B
虽然肿瘤坏死因子等细胞因子长期以来一直被认为是正常大脑生理所必需的，但它们在大脑中长期过量产生的影响现在也越来越多地被认识到。疟疾和铅中毒等各种症状，以及非传染性神经退行性疾病，都说明了这一点。这些细胞因子还协调大多数神经退行性变状态中tau、α-突触核蛋白、淀粉样蛋白-β水平和胰岛素抵抗程度的变化。关于间接抗肿瘤坏死因子药物沙丁胺醇对α-突触核蛋白和帕金森病的影响的新数据，极大地增加了了解和治疗这些疾病的抗肿瘤坏死因子方法的基本原理。正在测试的治疗进展，可以说对许多神经退行性疾病有用，包括减少过量的脑肿瘤坏死因子，无论是直接通过巴特森神经丛使用特定的抗肿瘤坏死因子生物制剂如依那西普，还是通过外科植入干细胞间接减少。吸入沙丁胺醇也需要对神经退行性疾病谱进行进一步研究。现在是时候整合神经退行性疾病谱系中的这一系列新信息了，而不是继续通过个别疾病状态的透镜来看待它。
While cytokines such as TNF have long been recognized as essential to normal cerebral physiology, the implications of their chronic excessive production within the brain are now also increasingly appreciated. Syndromes as diverse as malaria and lead poisoning, as well as non‐infectious neurodegenerative diseases, illustrate this. These cytokines also orchestrate changes in tau, α‐synuclein, amyloid‐β levels and degree of insulin resistance in most neurodegenerative states. New data on the effects of salbutamol, an indirect anti‐TNF agent, on α‐synuclein and Parkinson's disease, APOE4 and tau add considerably to the rationale of the anti‐TNF approach to understanding, and treating, these diseases. Therapeutic advances being tested, and arguably useful for a number of the neurodegenerative diseases, include a reduction of excess cerebral TNF, whether directly, with a specific anti‐TNF biological agent such as etanercept via Batson's plexus, or indirectly via surgically implanting stem cells. Inhaled salbutamol also warrants investigating further across the neurodegenerative disease spectrum. It is now timely to integrate this range of new information across the neurodegenerative disease spectrum, rather than keep seeing it through the lens of individual disease states.
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影响因子：
5.4
作者：
Beatman, Erica L.;Massey, Aaron;Beckham, J. David
通讯作者：
Beckham, J. David
影响因子：
7.3
作者：
Alexander SP;Fabbro D;Kelly E;Marrion NV;Peters JA;Faccenda E;Harding SD;Pawson AJ;Sharman JL;Southan C;Davies JA;CGTP Collaborators
通讯作者：
CGTP Collaborators
影响因子：
8
作者：
Boivin, Michael J.;Bangirana, Paul;John, Chandy C.
通讯作者：
John, Chandy C.
影响因子：
7.3
作者：
Alexander SP;Christopoulos A;Davenport AP;Kelly E;Marrion NV;Peters JA;Faccenda E;Harding SD;Pawson AJ;Sharman JL;Southan C;Davies JA;CGTP Collaborators
通讯作者：
CGTP Collaborators
影响因子：
4
作者：
Aizman I;Vinodkumar D;McGrogan M;Bates D
通讯作者：
Bates D