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Abstract #0613

Striatal Glutathione Deficit in Parkinson’s Disease Measured In Vivo with J-edited  1H MRS Directly Implicates Oxidative Stress in Disorder Pathophysiology

Dikoma C. Shungu1, Xiangling Mao1, Nora Weiduschat1, Aneliya Hanineva 2, Yize Zhao3, Halinder S. Mangat2, Guoxin Kang1, James Carter2, Natalie Hellmers2, and Claire Henchcliffe 2

1Radiology, Weill Cornell Medicine, New York, NY, United States, 2Neurology and Neuroscience, Weill Cornell Medicine, New York, NY, United States, 3Healthcare Policy and Research, Weill Cornell Medicine, New York, NY, United States

Postmortem studies of Parkinson’s disease (PD) brain have consistently reported deficits of nigrostriatal glutathione (GSH) – the most abundant antioxidant in living tissue – of up to 40% compared to normal brain, strongly implicating oxidative stress in the pathophysiology of PD. However, direct evidence corroborating a striatal GSH deficit in PD brain in vivo is currently lacking. Using J-edited 1H MRS, this study measured striatal GSH in vivo in patients with PD and in matched control subjects, and found not only a 15% deficit of striatal GSH in PD that corroborated postmortem data, but also evidence of nigrostriatal neurodegeneration in the disorder.


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