Longitudinal Measurements of Glucocerebrosidase activity in Parkinson's patients.

Autor: Alcalay, Roy N.¹ (AUTHOR) rna2104@columbia.edu, Wolf, Pavlina² (AUTHOR), Chiang, Ming Sum Ruby³ (AUTHOR), Helesicova, Karolina² (AUTHOR), Zhang, Xiaokui Kate² (AUTHOR), Merchant, Kalpana⁴ (AUTHOR), Hutten, Samantha J.⁵ (AUTHOR), Scherzer, Clemens^6,7,8 (AUTHOR), Caspell‐Garcia, Chelsea⁹ (AUTHOR), Blauwendraat, Cornelis¹⁰ (AUTHOR), Foroud, Tatiana¹¹ (AUTHOR), Nudelman, Kelly¹¹ (AUTHOR), Gan‐Or, Ziv^12,13,14 (AUTHOR), Simuni, Tanya⁴ (AUTHOR), Chahine, Lana M.¹⁵ (AUTHOR), Levy, Oren¹ (AUTHOR), Zheng, Dandi¹⁶ (AUTHOR), Li, Gen¹⁶ (AUTHOR), Sardi, Sergio Pablo³ (AUTHOR), Marek, Kenneth (AUTHOR)

Publikováno v: Annals of Clinical & Translational Neurology. Oct2020, Vol. 7 Issue 10, p1816-1830. 15p.

Longitudinal Measurements of Glucocerebrosidase activity in Parkinson's patients

Autor: Alcalay, Roy N, Wolf, Pavlina, Chiang, Ming Sum Ruby, Helesicova, Karolina, Zhang, Xiaokui Kate, Merchant, Kalpana, Hutten, Samantha J, Scherzer, Clemens, Caspell-Garcia, Chelsea, Blauwendraat, Cornelis, Foroud, Tatiana, Nudelman, Kelly, Gan-Or, Ziv, Simuni, Tanya, Chahine, Lana M, Levy, Oren, Zheng, Dandi, Li, Gen, Sardi, Sergio Pablo, Parkinson’s Progression Markers Initiative

Publikováno v: Annals of clinical and translational neurology, vol 7, iss 10

ObjectiveReduction in glucocerebrosidase (GCase; encoded by GBA) enzymatic activity has been linked to Parkinson's disease (PD). Here, we correlated GCase activity and PD phenotype in the Parkinson's Progression Markers Initiative (PPMI) cohort.Metho

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_______325::4b85232aa49dde9a367bf06ce0b88eb1
https://escholarship.org/uc/item/492590bj

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Membrane trafficking and mitochondrial abnormalities precede subunit c deposition in a cerebellar cell model of juvenile neuronal ceroid lipofuscinosis

Autor: Cattaneo Elena, Rigamonti Dorotea, Gao Hanlin, Teed Allison M, Lubicz-Nawrocka Tanya, Espinola Janice A, Wolf Pavlina, Fossale Elisa, MacDonald Marcy E, Cotman Susan L

Publikováno v: BMC Neuroscience, Vol 5, Iss 1, p 57 (2004)

Abstract Background JNCL is a recessively inherited, childhood-onset neurodegenerative disease most-commonly caused by a ~1 kb CLN3 mutation. The resulting loss of battenin activity leads to deposition of mitochondrial ATP synthase, subunit c and a s

Externí odkaz: https://doaj.org/article/269535263e8c40eb9a23794e995de91d

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