Journal
JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
Volume 51, Issue 5, Pages 535-549Publisher
WILEY
DOI: 10.1111/j.1469-7610.2009.02187.x
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Funding
- National Institutes of Health [AA016548, DA009457, MH056539, MH068582, MH073725, MH081177]
- Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development
- NARSAD
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH056539, R29MH056539, R01MH073725, R01MH081177, P50MH068582] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R21AA016548] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA009457] Funding Source: NIH RePORTER
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The onset of diagnostic symptomology for neuropsychiatric diseases is often the end result of a decades-long process of aberrant brain development. Identification of novel treatment strategies aimed at normalizing early brain development and preventing mental illness should be a major therapeutic goal. However, there are few models for how this goal might be achieved. This review uses the development of a psychophysiological correlate of attentional deficits in schizophrenia to propose a developmental model with translational primary prevention implications. Review of genetic and neurobiological studies suggests that an early interaction between alpha 7 nicotinic receptor density and choline availability may contribute to the development of schizophrenia-associated attentional deficits. Therapeutic implications, including perinatal dietary choline supplementation, are discussed.
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