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Aging is associated with a reduction of brain plasticity and learning ability. Using a translational approach with investigations on animals, and on human subjects we investigate whether and how plasticity in the aged brain can be preserved. For this purpose, we use different approaches (telomere length, transcriptomic profile, MRI brainage score, neuropsychological parameters) to determine the biological age of subjects. Aging experiments with rodents show that prenatal stress induces an epigenetic alteration of the stress axis which enhances the inflammation level in the brain. Likewise, strong intermittent inflammatory disorders accelerate brain aging. Antiinflammtory drugs may partially reverse the age-associated disturbances of brain plasticity. Similarly, enriched environment partially re-juvenates the transcriptomic profile of the brain. Based on these observations we currently investigate the role of brain microglia for brain ageing. In the presentation, the methodological approach as well as results from several studies which address interventions to reduce the age-associated decline in brain plasticity will be presented.
Determinism is a special property of some systems and is defined by its state-space behavior in which the trajectories in time never intersect. Whether or not determinism exists in brain activities is a question that may be resolved by analysis of the dynamical properties of the electroencephalogram (EEG) or magnetoencephalogram (MEG). We will show that even though there are strong nonstationarities in most brain behaviors, small epochs of deterministic dynamics can still be observed. We will also show that the local Lyapunov exponents are measures that can demonstrate smooth transitions into these deterministic states.
The effects of photothrombotic stroke in primary somatosensory cortex on astroglial and microglial activation in various regions of lesioned brain were examined at different time points, using immunohistochemistry and lectin binding. The increase in GFAP expression was observed exclusively in the ipsilateral hemisphere, both in the perilesional area and cortical regions distant from the infarct. This remote increase was detectable up to sixty days after the infarct. Transient GFAP elevation was also found in the hippocampus one day after photothrombosis, whereas it was more prolonged in amygdala, as demonstrated at four days after lesion. In contrast to a widespread astrocytic activation, the microglial response was shortlasting and local, confined to lesion and perilesional area. Widespread and prolonged activation of astrocytes after stroke may provide factors promoting slowly developing recovery processes in the whole brain, while microglial response seems to be involved in local repair and removal of cellular debris.
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