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Furthermore, another component of the API complex, FOSL1, is highly expressed in IPSC-derived motor neurons from SOD1 patients carrying the E100G mutation (Bhinge et al., 2017) compared to isogenic controls, suggesting that the AP1 complex is a driver for neurodegeneration

In a similar vein, Kims team demonstrated that EA at ST36 can inhibit the occurrence of peripheral inflammation by activating postganglionic sympathetic neurons (111, 112)

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