Adult reversal of cognitive phenotypes in neurodevelopmental disorders
Open Access
- 17 June 2009
- journal article
- research article
- Published by Springer Nature in Journal of Neurodevelopmental Disorders
- Vol. 1 (2), 150-157
- https://doi.org/10.1007/s11689-009-9018-7
Abstract
Recent findings in mice suggest that it is possible to reverse certain neurodevelopmental disorders in adults. Changes in development, previously thought to be irreparable in adults, were believed to underlie the neurological and psychiatric phenotypes of a range of common mental health problems with a clear developmental component. As a consequence, most researchers have focused their efforts on understanding the molecular and cellular processes that alter development with the hope that early intervention could prevent the emergent pathology. Unexpectedly, several different animal model studies published recently, including animal models of autism, suggest that it may be possible to reverse neurodevelopmental disorders in adults: Addressing the underlying molecular and cellular deficits in adults could in several cases dramatically improve the neurocognitive phenotypes in these animal models. The findings reviewed here provide hope to millions of individuals afflicted with a wide range of neurodevelopmental disorders, including autism, since they suggest that it may be possible to treat or even cure them in adults.Keywords
This publication has 70 references indexed in Scilit:
- Disrupted in Schizophrenia 1 Regulates Neuronal Progenitor Proliferation via Modulation of GSK3β/β-Catenin SignalingCell, 2009
- Response of a Neuronal Model of Tuberous Sclerosis to Mammalian Target of Rapamycin (mTOR) Inhibitors: Effects on mTORC1 and Akt Signaling Lead to Improved Survival and FunctionJournal of Neuroscience, 2008
- Biological markers of intellectual disability in tuberous sclerosisPsychological Medicine, 2007
- Timing of Thyroid Hormone Action in the Developing Brain: Clinical Observations and Experimental FindingsJournal of Neuroendocrinology, 2004
- Chromatin Acetylation, Memory, and LTP Are Impaired in CBP+/− MiceNeuron, 2004
- Function and Regulation of CREB Family Transcription Factors in the Nervous SystemNeuron, 2002
- A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndromeNature Genetics, 2001
- PTEN Mutation Spectrum and Genotype-Phenotype Correlations in Bannayan-Riley-Ruvalcaba Syndrome Suggest a Single Entity With Cowden SyndromeHuman Molecular Genetics, 1999
- Local GABA Circuit Control of Experience-Dependent Plasticity in Developing Visual CortexScience, 1998
- Identification and characterization of the tuberous sclerosis gene on chromosome 16Cell, 1993