Stroke

Dr. Lifshitz is the Director of the Translational Neurotrauma Research Program through the College of Medicine - Phoenix, which brings together clinicians and scientists as faculty to address the pathophysiology and recovery from animal models of acquired neurological injury (e.g. stroke, hemorrhage, concussion). These studies are guided by gaps in clinical knowledge to empower healthcare providers to improve quality of life for survivors. To this end, they use public databases, biorepositories, and animal models to address questions across the lifespan. Specific strengths include inflammation, rehabilitation, puberty, sleep, and neuronal morphology.

My research program is centered on investigating the neurobiology of healthy language system, and changes in cognitive and language processing associated with stroke and neurological disorders. My interests include incorporating cognitive measures and multimodal neuroimaging methods, with a goal to understand the relationship between language and other aspects of cognition, as well as the neural dynamics related to brain damage, resilience, and recovery. My research efforts are directed towards identifying factors which affect language comprehension and production, and how these change with development and are influenced by aging, stroke, brain injury, and neurodegenerative disorders, including Primary Progressive Aphasia (PPA) and Alzheimer’s disease (AD). I study language processing at the multiple levels, using behavioral experiments and both structural (DTI, lesion-symptom mapping, voxel-based morphometry) and functional neuroimaging (fMRI, EEG, MEG). In addition, I am interested in neuroplasticity and application of noninvasive brain stimulation techniques (e.g., TMS, tDCS) to the treatment of aphasia and dementia. The long-term goal of my research is to understand the cognitive and neural processes that support recovery of cognitive and language functions after stroke. Keywords: stroke, aphasia, dementia, MRI, EEG, Language

The Doyle lab investigates the role of the immune system in causing dementia after stroke. Up to 30% of stroke patients develop dementia in the months and years after their stroke and we are testing the hypothesis that in some patients this is due to a chronic inflammatory response that persists at the site of the stroke infarct. We suspect that in the weeks, months and possibly years after stroke, neurotoxic inflammatory mediators, including T cells, cytokines and antibodies, leak out of the stroke infarct and cause bystander damage to the surrounding tissue, which then both impairs recovery, and in some instances leads to cognitive decline. In support of this hypothesis we have data that demonstrates that inflammation persists for months at the site of the infarct after stroke, and that a single stroke can directly lead to the development of immune-mediated delayed cognitive deficits. We are currently in the process of targeting different components of the prolonged inflammatory response to stroke to determine if post stroke dementia can be treated by selectively ablating individual immune mediators such as B lymphocytes, T lymphocytes, and CCR2. Keywords: Neuroinflammation, stroke, dementia, Alzheimer's disease