Manipulating inflammation and gliosis in neurological diseases-a clinical perspective
In many neurological diseases, an infl ammatory reaction in the brain is observed. In some of them, as in multiple sclerosis, the brain infl ammation is a result of a systemic autoimmune response. In others, like the Parkinson’s disease, Alzheimer’s disease, brain injury and stroke, an infl ammation and glial proliferation in the brain are a secondary phenomenon to neural degeneration or injury. The role of these reactions in the pathogenesis of neurological diseases is unclear. From one side they can contribute to greater neurological defi cit. From the other side, infl ammatory cells may release trophic factors and contribute to neuroprotection and neuroregenaration. Experimental works provide some evidences that pharmacological inhibition of brain infl ammation and glial proliferation may be protective but also may be harmful. The infl uence of anti-infl ammatory therapies on the progression of neurological diseases depends on a dose and time of the treatment after injury. Therefore, a clinical use of drugs infl uencing infl ammation and glial proliferation is very diffi cult. Despite many anti-infl ammatory therapies used in neurological diseases at present, there is no clinical evidence of their benefi cial effects. Various immunomodulatory therapies have been tested in multiple sclerosis, but only some modest modifi cations of clinical course are observed. Similarly, in neurodegeneration like in the Parkinson’s disease, non-steroidal anti-infl ammatory drugs do not change disease progression.