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This higher activity results from the insensitivity of ETC to FCCP treatment and is consistent with the limited reserve capacity of Gclc -deficient FoB (Fig

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Cerebroside (CEGI) reduces A deposition and ameliorates cognitive dysfunction in APPswe/PS1dE9 AD model mice by decreasing the level of PSD-95 palmitoylation while up-regulating the expression of synaptic proteins, such as NR2B, SYT1, and PSD-95, in the frontal cortex (176)