The dynamic nature of brain function is dependent on brain plasticity, i.e. on the remodeling of neuronal connectivity in response to sensory input. Following brain injury, brain plasticity becomes important during recovery of lost brain function and encompass wound healing, synaptogenesis and activation of new neuronal network. In this project we aim to identify mechanisms that stimulate recovery of the surviving tissue after injury. Specifically, we study the spine dynamics in the peri-infarct area, regenerative cross-talk between injured neurons and reactive astrocytes around the injury site and between astrocytes and inflammatory cells during scar formation.
Mild therapeutic hypothermia is presently the only treatment that attenuates brain dysfunction after brain ischemia in patients. This neuroprotective effect is readily studied in models of experimental brain ischemia and in cell and tissue cultures. The Laboratory for Experimental Brain Research has pioneered the studies of hypothermic brain protection. Our studies suggest that the protective mechanism of hypothermia involves mitigating processes regulated by the actin cytoskeleton. In this project we aim to identify the cellular and molecular mechanisms of hypothermic brain protection.
Ischemic cell death subsequent to stroke is a rapid process that also continues over several days after the brain injury. inflammation surges at the site of the ischemic lesion as a response to ischemia and inflammatory cells are activated and accumulate in the ischemic area. In this project we study the stroke-induced inflammatory cascades and its role and action in neuronal death/survival. We are particularly interested in the temporal sequence of events during inflammation and how could these mechanisms be manipulated to ameliorate the injury?
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Last modified: 2008-09-10
