The glutamate-based genetic immune hypothesis in obsessive-compulsive disorder. An integrative approach from genes to symptoms.
Neuroscience. 2010-01-01; 165(2): 408-417
DOI: 10.1016/j.neuroscience.2009.10.043
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1. Neuroscience. 2010 Jan 20;165(2):408-17. doi:
10.1016/j.neuroscience.2009.10.043.
The glutamate-based genetic immune hypothesis in obsessive-compulsive disorder.
An integrative approach from genes to symptoms.
Rotge JY(1), Aouizerate B, Tignol J, Bioulac B, Burbaud P, Guehl D.
Author information:
(1)Laboratoire Mouvement Adaptation Cognition, CNRS UMR 5227, Université
Bordeaux 2, Bordeaux, France.
Recent advances in multiple areas of research have contributed to the
identification of several pathophysiological factors underlying
obsessive-compulsive disorder (OCD). In particular, the glutamate transporter
gene SLC1A1 has been associated with the diagnosis of OCD. Immunological and
infectious studies have reported alterations of the immune system and the
presence of immune complexes directed against the Borna disease virus in OCD
patients. In addition, neuroimaging of OCD patients has demonstrated
abnormalities in the anterior cingulate cortex, orbitofrontal cortex, thalamus,
and the basal ganglia. Neuropsychological assessments have found several
cognitive disruptions that have been identified in OCD, especially impairments
in cognitive flexibility. Here, we attempt to bridge the gap between these
remarkable findings through several previously unpredicted pathophysiological
mechanisms. We propose an integrative hypothesis that indicates how genetic and
environmental factors may contribute to the structural and functional
alterations of cortico-subcortical circuits, leading to the characteristic
cognitive disruptions underlying OCD symptoms.
DOI: 10.1016/j.neuroscience.2009.10.043
PMID: 19861150 [Indexed for MEDLINE]