Doesn’t mention schizophrenia directly but does mention DISC1 (Disrupted in Schizophrenia1)
There are now a number of compelling examples, in mice, of rescue of neurocognitive deficits associated with developmental disorders in adults , including NF1, TSC, Down syndrome, Rubinstein-Taybi syndrome (RTS), Fragile X syndrome (FXS), and Rett syndrome.
This part is about Rett syndrome:
The analysis of a number of phenotypes caused by the Mecp2 mutation, including hind limb clasping, inertia, irregular breathing, gait, and tremor, showed that these phenotypes were not irreversible even in adults. Accordingly, restoring Mecp2 expression in mature female mutant mice, after onset of neurological disease, reversed function to wild-type levels and restored proper levels of neuronal plasticity. Interestingly, sudden restoration of Mecp2 function actually caused death in half of the mice treated, while a more gradual re-expression schedule did not. This result suggests that the dynamic (although precarious) biochemical balance established in mutant mice had to be reversed in a progressive gradual manner. Additionally, it is important to note that restoration of normal Mecp2 expression only took place in approximately 80% of cells, demonstrating that complete reversal is not needed for significant gains in function. This is a key result with significant repercussions for possible future clinical studies with viral vectors where only a subset of cells may be expected to be transfected. These fascinating findings demonstrate that deficits caused by loss of Mecp2 function in development do not result in irrevocable impairments.