Does inflammation after stroke depend on age?
Brain ischemia or stroke is an important worldwide health issue. Administration of tissue plasminogen activator (tPA) constitutes an efficient treatment that, however, can only be applied within a certain time window following stroke. This necessitates the development of treatment strategies for brain protection beyond this early time frame. There are many indications that the events in the brain following a stroke are age-dependent. Strategies for neuro-protection have failed possibly due to flaws in the design of the original studies. Emerging clinical trial results show a strong association between post-stroke infections and neurological outcome. With this in mind, the 'Age-dependent inflammatory responses after stroke' (Arges) project aimed to characterise any age-dependent changes of local and systemic immune responses following stroke. To achieve that they used an animal model and performed vast transcriptional, proteomic and biochemical analyses. Using whole genome arrays, project partners were able to identify genes and pathways that are significantly affected by stroke in combination with ageing. The association of stroke and immunity came from the finding that regulation of microglial cells – the immune cells of the central nervous system – was altered after stroke. This clearly suggested that following stroke the immune balance becomes disturbed. The project was able to define novel genes and proteins responsible for age-dependent recovery and to characterise the post-stroke inflammatory response. Overall, the study provided an in-depth characterisation of immune responses occurring after stroke and, combined with patient data, study findings have the potential to pave the way for improved diagnosis and therapies in elderly patients. Applications of these research results may include new age-adjusted therapeutic options to reduce the effects caused by inflammation and systemic immune suppression after the stroke.
