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The peptides anxiolytic mechanism appears to involve favoring natural homeostasis of the GABA receptor complex and enhancing GABAergic transmission through distinct, non-benzodiazepine pathways

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However, only one channellocalized opposite to the nonheme ironexhibits high oxygen affinity at the active site (Saam et al

Studies in AD brains have shown that Uch-L1 deficits are linked to the accumulation of A in the ascending gracile tract as demonstrated by a mouse model of gracile axonal dystrophy (GAD

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