The opioid epidemic in the United States is a national public health crisis, with opioid-related overdoses contributing to more than 75% of drug overdose deaths. Despite the prevalence of opioid use disorders (OUD), available treatment options remain limited, and there is a critical need to develop novel therapeutics. Opioid addiction is mediated, in part, by mu opioid receptors (MOR) in the ventral tegmental area (VTA). The primary goal of my research is to determine how the neuropeptide galanin interacts with MOR signaling in the VTA to regulate opioid reward using a combination of chemogenetics, RNAscope in situ hybridization, immunohistochemistry, and conditioned place preference behavior.
I am interested in understanding the role of the locus coeruleus (LC) in Alzheimer’s disease (AD). The LC exhibits hyperphosphorylated tau prior to any other brain region, causing disrupted noradrenergic function which may contribute to prodromal neuropsychiatric symptoms, progression to cognitive impairment, and the spread of tau pathology. I am using both human and mouse models to understand how early changes in the LC affect AD, which may lead to earlier diagnosis, treatment, and better patient outcomes.
I am interested in the underlying pathophysiology of major psychiatric disorders, with a focus on bipolar disorder (BD). Our selectively bred Hyperactive (HYPER) rat model reflects the oscillating nature of BD through pronounced outbursts of hyperactivity and psychomotor retardation. Using genetic and molecular techniques, I am identifying underlying mechanisms responsible for the HYPER rat phenotypes. My ultimate goal is to improve our understanding of the neurobiology of neuropsychiatric disorders and to identify potential molecular targets.
My research is focused on the locus coeruleus (LC) in neurodegeneration, focusing on the pigment-like substance neuromelanin (NM). My research aims to understand how changes in neuronal activity and metabolism influence the aggregation of NM and subsequent degeneration of LC neurons.
The neurobiological basis of prodromal symptoms such as sleep disruptions, anxiety, depression, and agitation in Alzheimer's disease (AD) are relatively unappreciated. Given that an early pathological feature of AD is presence of hyperphosphorylated tau in the locus coeruleus, I am interested in untangling the LC-specific mechanisms governing prodromal phenotypes in AD. To probe this question, I will be utilizing a combination of mouse genetics, immunohistochemistry, and behavioral paradigms.
I am intrigued by the neurobiological and behavioral symptoms of Alzheimer’s Disease (AD) over time. By studying the effects of hyperphosphorylated tau accumulation in the mouse locus coeruleus, I hope to understand changes in attention, impulse behavior, and response inhibition. This approach will enable us to uncover the molecular processes responsible for the impairment of locus coeruleus function in AD.
Hyperphosphorylated tau in the locus coeruleus (LC) is the earliest detectable feature of Alzheimer’s disease (AD) pathology, often occurring decades before cognitive decline. I am interested in examining the functional impact of LC degeneration on behavior and neuropathology in a transgenic rat model of AD.
My research focuses on the impact of vesicular monoamine transporter 2 overexpression and norepinephrine transporter inhibition on neuromelanin (NM)-induced locus coeruleus (LC) neurodegeneration. By studying these mechanisms in mice, my goal is to provide insight into potential treatments targeted at reducing NM neurotoxicity, LC neurodegeneration, and the resulting non-motor symptoms of Parkinson’s Disease.