Schahram Akbarian

TL;DR: The results indicate that the role of MECp2 is not restricted to the immature brain, but becomes critical in mature neurons, and that Mecp2 deficiency in these neurons is sufficient to cause neuronal dysfunction with symptomatic manifestation similar to Rett syndrome.

TL;DR: The prefrontal cortex of schizophrenics shows reduced expression for GAD in the absence of significant cell loss, bringing about an activity-dependent down-regulation associated with the functional hypoactivity of the DLPFC and implying that overall cortical neuronal migration had not been compromised in development.

TL;DR: The resource and integrative analyses have uncovered genomic elements and networks in the brain, which in turn have provided insight into the molecular mechanisms underlying psychiatric disorders.

TL;DR: Findings are consistent with a disturbance of the subplate during development in which the normal pattern of programmed cell death is compromised and accompanied by a defect in the normal orderly migration of neurons toward the cortical plate, likely to have serious consequences for the establishment of anormal pattern of cortical connections leading to a potential breakdown of frontal lobe function in schizophrenics.

TL;DR: The histone deacetylase inhibitor SB exerts antidepressant-like effects in the mouse and the therapeutic benefits and molecular actions of histone modifying drugs, including co-treatment with SSRIs and other newer generation antidepressant medications, warrant further exploration in experimental models.