Rev Neurol. 2008 Jun 1-15;46(11):675-83.
Inflammatory/anti-inflammatory mechanisms in the brain following exposure to stress.
Garcia-Bueno B, Leza JC. Universidad Complutense. Facultad de Medicina, 28040 Madrid, Espana.
INTRODUCTION: Most of the biological systems that go to make up an organism can be affected by stress. The central nervous system not only plays an essential role in regulating the general response to stress, but it is also one of its main targets. The consequences may be positive (for example, a state of alertness) or negative (neuropsychiatric pathologies). More specifically, exposure to certain stressing stimuli can trigger a neuroinflammatory process.
DEVELOPMENT: Reports have appeared describing how an excessive neuroinflammatory response makes a decisive contribution to the functional and structural damage that is often observed in stress-related neurological and neuropsychiatric diseases, such as post-traumatic stress syndrome, depression and schizophrenia. The inflammatory process generated by exposure to stress is characterised by a complex release of a chain of different cell mediators, such as cytosines, transcription factors, prostaglandins, free radicals, and so forth. In parallel to this, it has been proved that the anti-inflammatory pathway of deoxyprostaglandins is activated after stress in the central nervous system, and this activation could constitute an endogenous mechanism that regulates the inflammatory process itself.
CONCLUSIONS: In the future, further studies and a deeper understanding of this endogenous pathway could make it into a new, interesting preventive or neuroprotective strategy for use in a number of pathologies that have a clear harmful inflammatory component, such as cerebral ischaemia, Alzheimer's and Parkinson's diseases, as well as those mentioned earlier as being related to exposure to stress.
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