Schizophrenia Breakthrough

Scientists have recently identified a critical function of what they believe to be schizophrenia’s Matthew Ludwick schizophrenia“Rosetta Stone” gene, that could very well hold the key to decoding the function of all genes involved with the disease.  This breakthrough has revealed a vulnerable period in the early stages of the brain’s development, that researchers hope can be targeted for future efforts in reversing schizophrenia.  The researchers, from Cardiff University, published a paper in the journal Science that they say uncovered the previously-unknown influence of a gene in ensuring healthy brain development.

The gene in question is known as “disrupted schizophrenia-1” (DISC-1).  Previous studies have revealed that when mutated, this gene is a high-risk factor for mental illnesses such as major clinical depression, bipolar disorder and schizophrenia.  This latest study’s aim was to determine whether or not DISC-1’s interactions with other proteins in the earlier part of the brain’s development had a bearing on the brain’s ability to adapt its structure and function (aka “plasticity”) later on in adulthood.  Many genes that are responsible for creating synaptic proteins have been previously shown to be strongly linked to schizophrenia and other brain disorders, although until now these reason haven’t been properly understood.

The team found that in order for healthy development of the brain’s synapses to take place, the DISC-1 gene first needs to bind with two other molecules, known as “Lis” and “Nudel”.  Their experiences in mice revealed that through preventing DISC-1 from binding with these molecules with a protein-releasing drug called Tamoxifen at an early stage of the brain’s development, it would lack plasticity once it grows to its adult state.  This prevents cortical neurons in the brain’s largest region from being able to form synapses, damaging the ability to form coherent thoughts and properly perceive the world.

When the brain was fully formed, preventing DISC-1 from binding with “Lis” and “Nudel” molecules showed no effect on plasticity.  However, researchers could pinpoint a seven-day window early on in the brain’s development (one week after birth) where the failure to bind had an irreversible effect on the brain’s plasticity later on in life.  According to researchers, the challenge ahead lies in finding a way of treating people during this critical period, or in finding ways of reversing the problem during adulthood by returning plasticity to the brain.