Qin Wang

Scholarship

Selected Recent Publications

• Activation of a novel α(2A)AR-spinophilin-cofilin axis determines the effect of α(2) adrenergic drugs on fear memory reconsolidation., 2022
  Journal Article, Academic Journal
• Microglial NLRP3 inflammasome activates neurotoxic astrocytes in depression-like mice., 2022
  Journal Article, Academic Journal
• Differential requirement for DICER1 activity during the development of mitral and tricuspid valves., 2022
  Journal Article, Academic Journal
• A peptide blocking the ADORA1-neurabin interaction is anticonvulsant and inhibits epilepsy in an Alzheimer's model., 2022
  Journal Article, Academic Journal
• Self-paced five-choice serial reaction time-task for mouse behavior testing, 2022
  Journal Article, Academic Journal

Research Interests

Dr. Qin Wang's research interests revolve around investigating cell surface receptor signaling and neuropharmacology in the context of brain physiology and disease pathology. Her laboratory employs state-of-the-art techniques, including CRISPR editing, multiomic analysis, super-resolution imaging, pharmacological and behavioral approaches, as well as humanized animal models, human postmortem tissues, and iPSC-derived brain cells, to elucidate the molecular and cellular mechanisms underlying Alzheimer's disease (AD) and complex behaviors. Furthermore, the lab explores the therapeutic potential of targeting these mechanisms for disease treatment, with the ultimate goal of translating their fundamental discoveries into novel clinical applications. One of the primary focuses of Dr. Wang's lab is AD, a multifaceted disease that involves numerous genetic and environmental factors. Her lab employs a multifaceted approach to address this complexity, with a particular emphasis on the following areas: 1) exploring the contribution of noradrenergic dysfunction to AD pathogenesis; 2) investigating alterations in endosomal trafficking in AD and the interactions between AD risk factors; 3) elucidating the role of astrocytic signaling and reactivity in AD progression; 4) examining the relationship between AD risk and cancer therapies, as well as congenital heart diseases; 5) developing treatments for AD by targeting neuronal hyperexcitability.