TY - JOUR
T1 - Over-inhibition
T2 - a model for developmental intellectual disability
AU - Fernandez, Fabian
AU - Garner, Craig C.
N1 - Funding Information:
We thank the National Science Foundation (F.F.), the National Institute of Health (F.F.) the Down's syndrome Research and Treatment Foundation (C.C.G.), the Hillblom Foundation (C.C.G.), as well as the Stanford Down syndrome Center (C.C.G.) for their support. We would also like to thank M. Blank and R.J. Reimer for a critical reading of the manuscript.
PY - 2007/10
Y1 - 2007/10
N2 - Developmental intellectual disability (DID) is a daunting societal problem. Although tremendous progress has been made in defining the genetic causes of DID, therapeutic strategies remain limited. In particular, there is a marked absence of a unified approach to treating cognitive impairments associated with DID. Here, we suggest that the brain in many DID-related disorders is subject to a basic imbalance in neuronal activity, with an increased contribution of inhibition to neural circuits. This over-inhibition, in turn, is predicted to lead to deficits in synaptic plasticity and learning and memory. We further discuss possibilities for pharmacological intervention in DID, focusing on the concept of drug-induced 'therapeutic neuroadaptation' as a means of stably enhancing constitutive circuit excitability and cognition over time.
AB - Developmental intellectual disability (DID) is a daunting societal problem. Although tremendous progress has been made in defining the genetic causes of DID, therapeutic strategies remain limited. In particular, there is a marked absence of a unified approach to treating cognitive impairments associated with DID. Here, we suggest that the brain in many DID-related disorders is subject to a basic imbalance in neuronal activity, with an increased contribution of inhibition to neural circuits. This over-inhibition, in turn, is predicted to lead to deficits in synaptic plasticity and learning and memory. We further discuss possibilities for pharmacological intervention in DID, focusing on the concept of drug-induced 'therapeutic neuroadaptation' as a means of stably enhancing constitutive circuit excitability and cognition over time.
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U2 - 10.1016/j.tins.2007.07.005
DO - 10.1016/j.tins.2007.07.005
M3 - Article
C2 - 17825437
AN - SCOPUS:34848891591
VL - 30
SP - 497
EP - 503
JO - Trends in Neurosciences
JF - Trends in Neurosciences
SN - 0378-5912
IS - 10
ER -