Deidda G, Parrini M, Naskar S, Bozarth IF, Contestabile A, Cancedda L.
Reversing excitatory GABAAR signaling restores synaptic plasticity and memory in a mouse model of Down syndrome.
Nat Med. 2015 Mar 16;
PubMed.
Michael Rafii University of Southern California Keck School of Mediicine
Posted:
This is an elegant series of experiments, whereby Deidda et al. have identified the cation chloride co-transporter as a potential therapeutic target in Down’s syndrome (DS). Intriguingly, they have discovered that GABA receptor signaling is excitatory rather that inhibitory in the Ts65Dn mouse, and that modulation with an FDA-approved compound restores normal synaptic function and improves cognition. Knowing that dysfunction in the GABAergic system underlies certain aspects of intellectual disability in DS, this further supports the idea that the GABAergic system may be readily amenable to pharmacological intervention to improve cognition in DS.
Comments
University of Southern California Keck School of Mediicine
This is an elegant series of experiments, whereby Deidda et al. have identified the cation chloride co-transporter as a potential therapeutic target in Down’s syndrome (DS). Intriguingly, they have discovered that GABA receptor signaling is excitatory rather that inhibitory in the Ts65Dn mouse, and that modulation with an FDA-approved compound restores normal synaptic function and improves cognition. Knowing that dysfunction in the GABAergic system underlies certain aspects of intellectual disability in DS, this further supports the idea that the GABAergic system may be readily amenable to pharmacological intervention to improve cognition in DS.
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