Virtually all drug interventions that have been successful pre-clinically in experimental stroke have failed to prove their efficacy in a dinical setting. This could be partly explained by the complexity and heterogen...Virtually all drug interventions that have been successful pre-clinically in experimental stroke have failed to prove their efficacy in a dinical setting. This could be partly explained by the complexity and heterogeneity of human diseases as well as the associated co-morbidities which may render neuroprotective drugs less efficacious in dinical practice. One aspect of crucial importance in the physiopathology of stroke which is not completely understood is neuroinflammation. At the pres- ent time, it is becoming evident that subtle, but continuous neuroinflammation can provide the ground for disorders such as cerebral small vessel disease. Moreover, advanced aging and a number of highly prevalent risk factors such as obesity, hypertension, diabetes and atherosclerosis could act as ＂silent contributors＂ promoting a chronic proinflammatory state. This could aggravate the out- come of various pathological entities and can contribute to a number of subsequent post-stroke complications such as dementia, depression and neurodegeneration creating a pathological vicious cycle. Moreover, recent data suggests that the inflammatory process might be dosely linked with multiple neurodegenerative pathways related to depression. In addition, pro-inflammatory cyto- kines could play a central role in the pathophysiology of both depression and dementia.展开更多
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文摘Virtually all drug interventions that have been successful pre-clinically in experimental stroke have failed to prove their efficacy in a dinical setting. This could be partly explained by the complexity and heterogeneity of human diseases as well as the associated co-morbidities which may render neuroprotective drugs less efficacious in dinical practice. One aspect of crucial importance in the physiopathology of stroke which is not completely understood is neuroinflammation. At the pres- ent time, it is becoming evident that subtle, but continuous neuroinflammation can provide the ground for disorders such as cerebral small vessel disease. Moreover, advanced aging and a number of highly prevalent risk factors such as obesity, hypertension, diabetes and atherosclerosis could act as ＂silent contributors＂ promoting a chronic proinflammatory state. This could aggravate the out- come of various pathological entities and can contribute to a number of subsequent post-stroke complications such as dementia, depression and neurodegeneration creating a pathological vicious cycle. Moreover, recent data suggests that the inflammatory process might be dosely linked with multiple neurodegenerative pathways related to depression. In addition, pro-inflammatory cyto- kines could play a central role in the pathophysiology of both depression and dementia.
