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No heterogeneity was presented in the included studies (I 2 = 0%, P = 0.92), and we used the fixed effects model (Fig

The ZDHHC21T209S/T209S mouse model confirms that the mutation significantly increases neuronal excitotoxicity susceptibility and triggers synaptic dysfunction by enhancing FYN palmitoylation, leading to NMDAR2B overactivation and dysfunction and neuronal loss, ultimately resulting in cognitive deficits (168)

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