Does drebrin A reduction causally mediate NMDA receptor redistribution defects in presenilin knockout mice?

While the authors hypothesize that drebrin A loss explains NMDA receptor redistribution defects, this causal relationship is not directly tested. Establishing causality would validate drebrin A as a key mediator of presenilin-related synaptic dysfunction.

Gap type: open_question Source paper: Presenilin conditional double knockout mice exhibit decreases in drebrin a at hippocampal CA1 synapses. (None, None, PMID:22715045)

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