Weinshenker Lab Team

My research focuses on how interactions between the neuropeptide galanin and the endogenous opioid system drive behaviors associated with opioid reward, reinforcement, and withdrawal. My primary goal is to understand how and where galanin and opioid receptors interact to modulate, or mediate, these behaviors.

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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and a leading cause of death, with incidences likely to rise alongside an aging population. AD is characterized by aggregates of extracellular β-amyloid and intracellular tau neurofibrillary tangles. The locus coeruleus (LC) is the brain’s primary noradrenergic nucleus and is known to degenerate in various neurodegenerative disorders. Interestingly, the locus coeruleus is prone to hyperphosphorylated tau aggregation in AD, often decades prior to the onset of cognitive deficits. The goal of my research is to understand the effects of hyperphosphorylated tau on LC function using a combination of approaches including electrophysiology, optogenetics, and functional magnetic resonance imaging.

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I am a graduate student beginning my 4th year in the Molecular & Systems Pharmacology program. In the Weinshenker lab, I use mouse genetics, neuropharmacology, immunohistochemistry, and activity-dependent circuit mapping to interrogate the role of central norepinephrine transmission in the expression of anxious and compulsive behaviors. The goal of my research is to improve the current understanding of the neurobiology of anxiety disorders and to identify novel therapeutic targets and drug candidates to treat these conditions.

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I am interested in locus coeruleus (LC) dysfunction in Parkinson’s disease (PD). The LC is affected early and severely in PD, contributing to many of the non-motor symptoms patients experience.  My primary research goal focuses on investigating the transcriptional profile of noradrenergic neurons in the LC across disease stages. This will allow us to identify the underlying molecular mechanisms responsible for LC dysfunction in neurodegenerative disease.

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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. 

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My project focuses on the neuroanatomical basis of fear in mice by studying the role of genetically and pharmaceutically modified catecholamine levels in behavioral responses to predator odor. I hope to understand how norepinephrine and dopamine transmission contribute to anxiety and compulsive behaviors and identify new pharmaceutical targets for pathological fear.

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My research focuses on how modulation of the locus coeruleus impacts markers of Alzheimer's disease. I am currently focused on whether chronic LC activation can reduce Alzheimer's disease pathology and neuroinflammation in a transgenic rat model. Through this work, I hope to uncover novel therapeutics targeting the LC-NE system for use in Alzheimer's disease.

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