The research community has moved tentatively closer to identifying the roots of schizophrenia. Accumulated data reveals that a series of more than 50 source-unknown genetic mutations are three to four times as common among schizophrenic individuals. These mutations begin as early as conception or fetal development, disrupting basic genetic functions and most likely playing a profound role in the evolution of the disabled brain.
Using a groundbreaking "gene scanning" technology that can quickly create an overview of each individual human biogenetic map, researchers at the University of Washington and the National Institute of Mental Health examined groups of schizophrenic and control subjects, scanning for uncommon patterns in gene strands unique to given individuals and their immediate relatives. If any schizophrenic elements appeared in subjects' DNA profiles, they would most likely be here. Certain abnormal genetic profiles either lacked certain strands or contained duplicates of the same, and researchers found the incidence of schizophrenia to be far higher among those bearing these mutations. 5% of the control subject group bore some of the abnormalities in question, but they were present in 15% of the schizophrenic sample. Interestingly, individuals diagnosed with a rare, childhood-onset type of schizophrenia were even more likely (20%) to display the same set of abnormalities.
Previous most-probable-cause theories held that schizophrenia's origins could be found in a group of relatively common mutations. The theory read that, while these irregularities spawn less profound disorders on their own, they could create schizophrenia when present in certain simultaneous combinations. This study does not disprove such a pattern, but the mutations introduced could very well play a significant role in future research including the development of more efficient antipsychotic medications designed to target the individual irregularities as closely as possible. These mutations are not random, and most center around genes that play a central role in the brain's formation. One affected protein, for example, serves to guide neurons to their appropriate positions in the developing brain. Even slight variations in said protein could lead to dramatic structural changes in an affected individual's neurological framework.
Schizophrenia unquestionably has a genetic biological component as individuals whose siblings or parents have the disorder are far more likely to develop it themselves. But some experts point to these developments as further evidence of the relatively spontaneous nature of the condition which affects large, far-flung populations despite its many inherent evolutionary disadvantages. One cannot control for it, and it will persist despite all research until we can develop a counter-treatment.
This research, however promising, does not amount to a "gotcha" moment or a dramatic reversal of previously held opinions. In order to properly consider its potential influence, the individuals to which the results of this study apply must be considered as a share of the larger population. The large majority of schizophrenic patients do not, in fact, bear any of the mutations uncovered in this research. Of course, like all sterling research cases this study does not make any presumptions as to having identified the cause of the condition, but it certainly serves as a hopeful beacon and a marker from which to initiate any number of follow-up studies. The next key step in this progression will involve re-creating the irregularities observed in this study in order to better define their developmental origins and determine how best to address them. If nothing else, these studies highlight the enormous potential of gene scanning techniques. They will, in all likelihood, play a central role in the most groundbreaking treatment developments to emerge in the near future.
|