Weinshenker Lab Team

My research focuses on how tau in the locus coeruleus contributes to the progression of cognitive decline and pathological spread in a transgenic rat model of Alzheimer's disease. The goal of this research is to uncover new treatment targets for Alzheimer's disease, particularly in the early stages.

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I study opioid addiction, specifically how endogenous neuropeptides modulate responses to opioid exposure. I currently use a combination of genetic, cellular, and behavioral approaches to explore the effects of the neuropeptide galanin on opioid reward, reinforcement, and withdrawal.

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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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My project focuses on understanding the neurobiological mechanisms underlying stress-related neuropsychiatric disorders, like anxiety and depression. Specifically, I'm interested in determining the roles of norepinephrine and the neuropeptide galanin from the locus coeruleus in regulating behavioral responses to stress by using transgenic mice that lack norepinephrine and mice with noradrenergic-specific removal or overexpression of galanin in combination with optogenetics and behavioral paradigms. 

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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 goal of my project is to use behavioral and neuroanatomical techniques to investigate how the neuropeptide galanin suppresses opioid reward and reinforcement.

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My research focuses on the neuroprotective effects of a neuropeptide called galanin. Using mouse models of Alzheimer's Disease, I aim to determine if overexpression of locus coeruleus (LC)-derived galanin allows for enhanced survival of neurons in the LC and their projections to downstream targets throughout the brain. I am interested in learning about the therapeutic potential of galanin for treating neurodegenerative disease.

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