Research

The interests of UH-MIND members span three central research themes:

Marker, Mechanism & Target Discovery

Dementia and related neurological disorders, like epilepsy or Parkinson’s disease, often begin years before the apparent onset of symptomology. In fact, senile plaques in the brain start to form decades before any cognitive impairment. On the other hand, not every individual that has Alzheimer’s disease pathology exhibits cognitive, memory, or sensory losses. This suggests that, in addition to the known prion-like precursors of dementia, there are other, yet undiscovered markers, mechanisms, and targets that may be key in formation of dementia. A significant advantage of this team is access and expertise in using a variety of models, from in silico, to fruit flies, fish, to higher order species that can lead to novel discoveries and therapies.

Immune Dysregulation & Neurodegeneration

Immune dysfunction often forecasts or accompanies long-term physiological and cognitive brain changes. Traumatic brain injury, viral infections, and changes in the overall body’s and brain’s immune response can lead to excessive inflammation and exacerbate neurodegeneration in the brain. The role of neurons and glia in the brain is equally important. Recently, T cell dysfunction has been linked to Parkinson’s Disease pathogenesis, and neuron-specific T cells have the potential to directly cause neuron damage. It highlights the involvement of the adaptive immune dysfunction. This is an emerging field of study and our faculty will use their strengths in forming a team under this theme.

Genetic, Cognitive & Social Aging Studies

Genetic, cognitive, and social aging studies can bridge research from simple model systems, such as fruit flies, to behavioral studies and ultimately to human drug development. This team will have members interested in genetic and aging-related neurodegenerative diseases (trisomy X, Downs Syndrome, etc), cognitive decline associated with neurochemical and neuroanatomical damage, early onset dementia with traumatic brain injury, role of neuroimmune system response in exacerbating or remediating disease, inflammatory response and microglia/astroglia activation, conserved mechanisms operating across taxa that affect neural system function, operate in damage and restoration (regeneration) of function, interventions that delay the onset and progression of dementia related functional and behavioral impairments, and predictive diagnostics to identify early disease through genetic related propensities and altered transcription/translation processes related to dementia. The role of pollutants and the importance of a community of social support are also key components in disease onset and progression.