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Fasudil, a Rho kinase inhibitor, promotes the autophagic degradation of A53T α-synuclein by activating the JNK 1/Bcl-2/beclin 1 pathway
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A53T α-synuclein could decrease neurite outgrowth with enhanced Rho kinase activity.

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Fasudil could attenuate the neurite outgrowth injury caused by A53T α-synuclein.

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Fasudil could promote the autophagic degradation of A53T α-synuclein.

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The effect of fasudil was mediated by JNK/Bcl-2/beclin 1/Vps34 pathway.

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