TY - JOUR
T1 - Early Cognitive Experience Prevents Adult Deficits in a Neurodevelopmental Schizophrenia Model
AU - Lee, Heekyung
AU - Dvorak, Dino
AU - Kao, Hsin Yi
AU - Duffy, áine M.
AU - Scharfman, Helen E.
AU - Fenton, André A.
N1 - Funding Information:
This work was supported by NIMH grant R01MH084038-01 and a Young Investigator’s Award from NARSAD to A.A.F., and by NIMH grant MH090606 and NYS OMH support to H.E.S. We are grateful to Drs. Steven Silverstein and Daniel Weinberger for advice. H.L. collected and analyzed data and wrote the manuscript. D.D. analyzed data, H.-Y.K. performed preliminary experiments, A.D. and H.S. performed and analyzed histological studies, and A.A.F. designed and supervised research and wrote the manuscript. All authors discussed the results and manuscript.
PY - 2012/8/23
Y1 - 2012/8/23
N2 - Brain abnormalities acquired early in life may cause schizophrenia, characterized by adulthood onset of psychosis, affective flattening, and cognitive impairments. Cognitive symptoms, like impaired cognitive control, are now recognized to be important treatment targets but cognition-promoting treatments are ineffective. We hypothesized that cognitive training during the adolescent period of neuroplastic development can tune compromised neural circuits to develop in the service of adult cognition and attenuate schizophrenia-related cognitive impairments that manifest in adulthood. We report, using neonatal ventral hippocampus lesion rats (NVHL), an established neurodevelopmental model of schizophrenia, that adolescent cognitive training prevented the adult cognitive control impairment in NVHL rats. The early intervention also normalized brain function, enhancing cognition-associated synchrony of neural oscillations between the hippocampi, a measure of brain function that indexed cognitive ability. Adolescence appears to be a critical window during which prophylactic cognitive therapy may benefit people at risk of schizophrenia.
AB - Brain abnormalities acquired early in life may cause schizophrenia, characterized by adulthood onset of psychosis, affective flattening, and cognitive impairments. Cognitive symptoms, like impaired cognitive control, are now recognized to be important treatment targets but cognition-promoting treatments are ineffective. We hypothesized that cognitive training during the adolescent period of neuroplastic development can tune compromised neural circuits to develop in the service of adult cognition and attenuate schizophrenia-related cognitive impairments that manifest in adulthood. We report, using neonatal ventral hippocampus lesion rats (NVHL), an established neurodevelopmental model of schizophrenia, that adolescent cognitive training prevented the adult cognitive control impairment in NVHL rats. The early intervention also normalized brain function, enhancing cognition-associated synchrony of neural oscillations between the hippocampi, a measure of brain function that indexed cognitive ability. Adolescence appears to be a critical window during which prophylactic cognitive therapy may benefit people at risk of schizophrenia.
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U2 - 10.1016/j.neuron.2012.06.016
DO - 10.1016/j.neuron.2012.06.016
M3 - Article
C2 - 22920261
AN - SCOPUS:84865393422
SN - 0896-6273
VL - 75
SP - 714
EP - 724
JO - Neuron
JF - Neuron
IS - 4
ER -