{"id":4723,"date":"2016-08-15T14:57:00","date_gmt":"2016-08-15T18:57:00","guid":{"rendered":"https:\/\/www.med.unc.edu\/cellbiophysio\/directory\/natasha-snider-phd\/"},"modified":"2026-02-27T13:12:18","modified_gmt":"2026-02-27T18:12:18","slug":"natasha-snider-phd","status":"publish","type":"directory","link":"https:\/\/www.med.unc.edu\/cellbiophysio\/directory\/natasha-snider-phd\/","title":{"rendered":"Natasha Snider, PhD"},"content":{"rendered":"

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Associate Professor & CBP PhD Curriculum co-Director of Graduate Studies
\nUNC-Chapel Hill<\/p>\n

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Area of Interest<\/h2>\n

My research is focused on human diseases caused by defects in the cytoskeleton. The cytoskeleton is a key structural component of all cells that enables fundamental processes like growth, survival and movement. Abnormal remodeling of the cytoskeleton is prevalent across human diseases, including cancer and neurodegeneration. Our lab has generated clinically relevant human iPSC models to study the cell biology and pathology of cytoskeletal protein aggregates resulting from genetic mutations. We complement our human cell-based models with in vivo approaches aimed at preventing disease progression through the restoration of cytoskeletal proteostasis. Specifically, we focus on intermediate filaments (IFs), which form dynamic cytoskeletal networks critical for mechanical integrity, stress regulation, transcription, and proper organelle localization. IF gene mutations cause more than 80 human diseases that affect nearly every organ system and tissue type. Our current projects seek to advance the biology and therapy of two IF diseases that affect the nervous system: Alexander Disease (AxD) and Giant Axonal Neuropathy (GAN). Both diseases involve extensive IF protein accumulation and aggregation that harm glial and neuronal cells, leading to severe and progressive neurodegeneration. Understanding how neurons and glia degenerate in monogenic diseases like AxD and GAN will expand our understanding and repertoire of disease targets for other disorders and malignancies of the nervous system. The long-term goal for our research is to discover therapies for patients suffering from AxD, GAN and related IF diseases. We envision this can be done by using small molecule compounds in several ways, such as repurposing of existing drugs, targeting of post-translational modification enzymes (e.g. kinase inhibitors), or developing a new class of IF-specific drugs.<\/p>\n<\/div>\n

Find publications on PubMed<\/span><\/a><\/p>\n

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Awards and Honors<\/h2>\n