Schizophrenia: Clinical, neuropsychological and genetic correlations

International Congress on Neuroimmunology and Therapeutics

DoubleTree by Hilton Hotel San Francisco Airport, San Francisco, CA, USA

Lagouaiti Hanan

Posters-Accepted Abstracts: J Neurol Disord

Abstract :

Schizophrenia is a complex genetic disorder involving dysfunction in several brain regions, particularly the prefrontal and mesial temporal cortices and neurotransmitter systems such as glutamate. Evidence for cortical dysfunction has been observed by a variety of techniques. In prefrontal cortex, for example, patients exhibit cognitive, physiological and molecular alterations. Glutamatergic abnormalities have been inferred from several observations. In postmortem prefrontal cortex, alterations in several glutamate-related measures have been reported, including reduced mRNA levels of excitatory amino acid transporter 2 (EAAT2) also known as the glial glutamate transporter which plays an essential role in synaptic glutamate removal. These convergent findings suggest that some aspects of glutamate neurotransmission may be altered in prefrontal and mesial temporal regions in patients with schizophrenia and that these abnormalities could be partly genetic. Significant associations for complex genetic disorders such as schizophrenia often are difficult to replicate. This difficulty is not surprising given their presumed heterogeneity and the small effects of individual genes. Support for such associations can be enhanced by providing convergent biological and molecular evidence for functional effect of genes on pathophysiological mechanisms.