TY - GEN N2 - The abnormal accumulation of the intracellular protein a-synuclein has been implicated in the pathogenesis of several neurodegenerative disorders, including Dementia with Lewy Bodies (DLB), Lewy Body variant Alzheimer's Disease (LBVAD) & Parkinson's Disease (PD). In these diseases, known as synucleinopathies, the accumulation of aggregated a-synuclein in the cytoplasm, known as Lewy inclusions, is correlated with cellular dysfunction and death. Although the presence of Lewy inclusions are used as a marker for a definitive diagnosis of synucleinopathies, their specific role in neurodegeneration still remains unclear. The Unni lab has discovered a previously unrecognized function for the protein a-synuclein in repairing nuclear DNA damage. Based on this discovery, we have proposed a new hypothesis that during disease, a-synuclein protein is sequestered in cytoplasmic Lewy bodies, decreasing its nuclear DNA damage repair function and potentially leading to cell death of Lewy body-containing neurons. We have examined which confirmations of DNA a-synuclein preferentially binds for further insight into a-synuclein's normal function in the nucleus. DO - 10.6083/8336h2513 DO - DOI AB - The abnormal accumulation of the intracellular protein a-synuclein has been implicated in the pathogenesis of several neurodegenerative disorders, including Dementia with Lewy Bodies (DLB), Lewy Body variant Alzheimer's Disease (LBVAD) & Parkinson's Disease (PD). In these diseases, known as synucleinopathies, the accumulation of aggregated a-synuclein in the cytoplasm, known as Lewy inclusions, is correlated with cellular dysfunction and death. Although the presence of Lewy inclusions are used as a marker for a definitive diagnosis of synucleinopathies, their specific role in neurodegeneration still remains unclear. The Unni lab has discovered a previously unrecognized function for the protein a-synuclein in repairing nuclear DNA damage. Based on this discovery, we have proposed a new hypothesis that during disease, a-synuclein protein is sequestered in cytoplasmic Lewy bodies, decreasing its nuclear DNA damage repair function and potentially leading to cell death of Lewy body-containing neurons. We have examined which confirmations of DNA a-synuclein preferentially binds for further insight into a-synuclein's normal function in the nucleus. AD - Oregon Health and Science University AD - Oregon Health and Science University AD - Oregon Health and Science University T1 - Testing whether alpha-synuclein binds specific DNA conformations DA - 2020 AU - King, Dennisha AU - Dent, Elise AU - Unni, Vivek L1 - https://digitalcollections.ohsu.edu/record/8411/files/ResearchWeek.2020.King.Dennisha.pdf PB - Oregon Health and Science University LA - eng PY - 2020 ID - 8411 L4 - https://digitalcollections.ohsu.edu/record/8411/files/ResearchWeek.2020.King.Dennisha.pdf KW - alpha-Synuclein KW - Synucleinopathies KW - Neurodegenerative Diseases KW - Parkinson Disease KW - Lewy Body Disease KW - alpha-Synuclein KW - DNA Damage KW - lewy body dementias KW - lewy inclusions TI - Testing whether alpha-synuclein binds specific DNA conformations Y1 - 2020 L2 - https://digitalcollections.ohsu.edu/record/8411/files/ResearchWeek.2020.King.Dennisha.pdf LK - https://digitalcollections.ohsu.edu/record/8411/files/ResearchWeek.2020.King.Dennisha.pdf UR - https://digitalcollections.ohsu.edu/record/8411/files/ResearchWeek.2020.King.Dennisha.pdf ER -