Key mechanisms underlying damage and repair processes in sites of secondary neurodegeneration after ischemic stroke

This thesis investigates the processes involved in secondary neurodegeneration (SND), a chronic neuroinflammatory response to traumatic brain events, in areas remote from, but synaptically connected to, the primary site of insult. The work within (a) establishes the importance of environmental influences on stroke recovery by demonstrating that stress negatively modulates neurodegeneration in the thalamus, (b) provides a comprehensive review of the evidence supporting the proposal that stress is a necessary component of realistic recovery in animal models of experimental stroke, (c) characterises the temporal profile of neuroinflammation, neuron loss and neuron repopulation in thalamic SND, and (d) provides the first evidence that peripheral immune cells are present in sites of SND after stroke. This work provides novel insights into the phenomenon of SND that will assist future research in the development of a more thorough understanding of the processes regulating the chronic phase of recovery post-stroke and its potential for modulation.