The Thathiah Lab in the Department of Neurobiology at the University of Pittsburgh School of Medicine is recruiting two highly motivated postdoctoral associates to investigate the molecular and cellular mechanisms involved in Alzheimer's disease (AD) progression. Our lab studies AD mechanisms across molecular, cellular, and systems levels using human-derived induced neurons (iNs), glial models, and pre-clinical murine models. We integrate novel technologies to address hypothesis-driven questions in AD pathophysiology and advance the discovery of new therapeutic approaches. We seek individuals passionate about neuroscience and translational disease research who want to work in a collaborative, innovative environment and contribute to cutting-edge research with direct implications for AD therapies. Description of the Positions Neuroimmune Communication in Alzheimer's Disease. The first postdoctoral associate will lead an exciting, NIH-funded project investigating the role of neuroimmune signaling in AD. Specifically, the focus will be on our recent discovery of the G protein-coupled receptor (GPCR), GPR3, which is highly expressed in glial cells and may activate neuroprotective responses to AD pathology. This position offers the opportunity to study how neuroimmune interactions modulate disease progression in AD. Mechanisms of Tau Pathobiology in Alzheimer's Disease and Other Tauopathies. The second postdoctoral associate will spearhead an ongoing project to investigate the molecular mechanisms underlying pathological tau phosphorylation and aggregation. The lab has recently developed an optogenetic model of tau aggregation (optoTAU) that provides a unique platform for exploring tau aggregation across multiple cell types, including neurons, astrocytes, and oligodendrocytes. This project will focus on the cellular and molecular modifiers and the consequences of tau aggregation to better understand its role in AD pathogenesis.
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Job Type
Full-time
Education Level
Ph.D. or professional degree