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Our data indicate that the peptide treatment effectively reduced A accumulation and slowed down the clinical impairment of memory
Proposed Mechanisms Preventing GABA receptor downregulation Counteracting compensatory NMDA glutamate receptor sensitization Stabilizing benzodiazepine receptor configuration (preventing shift to inverse agonist state) Upregulating GABAergic neurotransmission through pathways distinct from benzodiazepine action itself This tolerance prevention has profound clinical implications

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