Clinical evidence shows that the identification of CHR individuals is possible via pre-emptive interventions to disrupt the formation of schizophrenia-like phenotype. More cellular studies dedicated to therapeutic mechanism are emerging for schizophrenia with promises on the reduction of schizophrenia-related anomalies (Millan, Andrieux, Bartzokis, & Cadenhead, 2016). The administration of regimen that interacts with GABAergic transmission or those that responds to stress is the new frontier for experiments and research. However, according to Millan et al. (2016), treatments that target intercellular protein, synaptic pruning, and epigenetic marking call for further characterisation. There is need for hybridisation of more than one regimen to relieve clinically high-risk (CHR) individuals of their symptoms. With developing epigenetics, targeting the underlying pathophysiology other than symptoms alleviation would be possible (Millan et al., 2016).
The criterion for evaluating data on schizophrenia susceptibility genes should be stringent as new findings show. It is encouraging that there are commonalities, relevant putative functions, and the replication of RGS4, neuregulin, and dysbindin. Nonetheless, each gene requires complete and independent replications for a firm acceptance. Chances of getting negative results are also probable as most replication samples lack power. The evidence on the growth of new gene pathways associated with single nucleotide polymorphisms (SNPs) require further investigation as the search for other schizophrenia genes via linkage and association methods. Genotype-phenotype correlations also need resolution to prove if schizophrenia and bipolar disorder are distinct genetically. The confirmation of genes susceptibility for schizophrenia would be a discovery to provide a skeleton clue on the pathophysiology of the disorder. The biochemical pathways and the molecular linkages it brings would be essential in proving the relevance of the disorder (Harrison, & Owen, 2003).
