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This premise is supported by studies showing that overexpressing Uch-L1 or pharmacologically enhancing Uch-L1 activity, improves long term potentiation (LTP) and cognition in AD transgenic mouse models (Gong et al., 2006), whereas knocking out Uch-L1 or pharmacologically inhibiting Uch-L1 causes a decline in cognition (Kurihara et al., 2001
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(2024) 11:e2307263
For example, an altered trace amine load (due to altered microbial composition or consumption of trace amine rich foods) and downstream trace aminergic signalling is anticipated in the ASD context but remains to be confirmed
