Striatal-enriched protein tyrosine phosphatase (STEP) has recently been implicated in several neuropsychiatric disorders with significant cognitive impairments, including Alzheimer’s disease, schizophrenia, and fragile X syndrome. A model has emerged by which STEP normally opposes the development of synaptic strengthening and that disruption in STEP activity leads to aberrant synaptic function. We review the mechanisms by which STEP contributes to the etiology of these and other neuropsychiatric disorders. These findings suggest that disruptions in STEP activity may be a common mechanism for cognitive impairments in diverse illnesses.
Keywords: STEP, protein tyrosine phosphatase, cognition, Alzheimer’s disease, fragile X syndrome, Huntington’s disease, schizophrenia, excitotoxicity
Citation: Fitzpatrick CJ and Lombroso PJ (2011) The role of striatal-enriched protein tyrosine phosphatase (STEP) in cognition. Front. Neuroanat. 5:47. doi: 10.3389/fnana.2011.00047
Received: 29 April 2011;
Accepted: 13 July 2011;
Published online: 29 July 2011.
Edited by:Emmanuel Valjent, Université Montpellier 1 & 2, France
Reviewed by:Joël Bockaert, INSERM, France
Copyright: © 2011 Fitzpatrick and Lombroso. This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
*Correspondence: Paul J. Lombroso, Laboratory of Molecular Neurobiology, 230 South Frontage Road, New Haven, CT 06520, USA. e-mail: email@example.com