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Ali Khoshnan, PhD, is Associate Professor of Research in Physiology and Neuroscience at the Zilkha Neurogenetic Institute, Keck School of Medicine of the University of Southern California. He received his PhD in Virology from the University of Texas Health Science Center in San Antonio in 1995. Khoshnan initiated his investigations into the molecular pathogenesis of Huntington's disease as a postdoctoral scholar under the late Professor Paul Patterson at the California Institute of Technology from 2000 to 2002, subsequently serving as a senior investigator there until 2022. He joined the University of Southern California in November 2022 to further his research on this neurodegenerative disorder caused by polyglutamine expansion in the huntingtin protein.
Khoshnan's laboratory employs human neurons, brain organoids, mouse, and Drosophila models to delineate pathogenic assemblies of mutant huntingtin, their propagation mechanisms, and neuronal pathways driving neurodegeneration. Efforts focus on engineering antibodies and nanobodies against pathogenic huntingtin conformations for diagnostic and therapeutic uses, alongside probing microbiota-gut-brain axis influences on Huntington's disease progression, including huntingtin's regulation of gut microbial homeostasis and pertinent gut-brain circuits. His contributions include pioneering therapeutic and diagnostic intrabodies, elucidating neuroinflammatory signaling pathways, generating antibodies targeting toxic huntingtin conformations, and uncovering prion-like amplification of neurotoxic species. He is a member of the Huntington's Disease Society of America Scientific Advisory Board. Select publications encompass "Gut Microbiota as a Modifier of Huntington’s Disease Pathogenesis" (Journal of Huntingtonton's Disease, 2024), "Epitope-specific antibodies can distinguish between soluble huntingtin exon-1 and its diverse cellular aggregates" (Journal of Biological Chemistry, 2026), "Amplification of neurotoxic HTTex1 assemblies in human neurons" (Neurobiology of Disease, 2021), "IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome" (Journal of Cell Biology, 2009), and "Activation of the IκB kinase complex and nuclear factor-κB contributes to mutant huntingtin neurotoxicity" (Journal of Neuroscience, 2004).

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