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. 2016 Jul 4;25(16):3432–3445. doi: 10.1093/hmg/ddw185

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© The Author 2016. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — GCase deficiency inhibits macroautophagy flux and increases α-synuclein protein levels in cortical neurons. (A) LC3B-II and p62 were measured in neurons under basal conditions, or following treatment with 100 nM Baf A1 for 6 h. LC3B-II and p62 levels were significantly increased in CBE-treated neurons (n = 7). (B) Intracellular total α-synuclein (n = 5) and phospho Ser129 α-synuclein (n = 6) were measured in neurons treated with CBE. (C) α-synuclein levels were measured in cell lysates (intracellular) and their respective conditioned cell culture media (extracellular) by ELISA. Data are from four independent neuron preps. All data represent mean ± S.E.M, * P < 0.05; ** P < 0.01 vs. respective control.