Above 21 million people in the world suffer from a mental disorder termed schizophrenia. It is characterized by language and thought disruption that create problems in the self-awareness and perception of patients. Common symptoms include hallucinations, delusions, disorganized behavior, depressed mood or irritability. Internally, the communication between the specialized brain cells called neurons is weak, where the gap in the synaptic communication between the neuron culminates in miscommunication; resulting in the distorted perception of reality.
Originally, modern research points in the direction of various genetic defects in the brain cells that contribute to this mental ailment. A combination of genetics, environmental factors, and improper brain chemistry are viewed as common causes behind it. However, a recent study by the University of Copenhagen suggests that the defect lies not in the neurons but in the glial cells, also known as the support cells of the brain. These glial cells are tasked to ensure the coordination of the synaptic communication between the neurons. When these support cells show disturbed progress or have undergone improper development during the formation of the brain, the miscommunication in the neurons occurs yielding schizophrenia.
This fresh study was conducted on mice whose brain cells were combined with human cells to produce a type of mice model named chimera. The human glial cells were embedded in the mouse brains and tested.
In its embryonic stage, the brain is formed in steps in accordance with a particular recipe. A specific type of stem cells called the progenitor cells, during this phase; develop into brain support cells that include astrocytes and oligodendrocytes. These cells play a crucial role in the formation and regulation of the network of neurons in the brain. The latter types of cells are particularly responsible for the production of myelin, the lack of which is believed to be the reason behind schizophrenia.
Defective glial cells also lead to an abnormal maturation of the brain. This is shown in the poor development of the white matter of the body’s central processing unit and the improper astrocyte development. Both of these factors contribute in impairing the information processing of the brain. The research showed that such changes in the brain resulted in excessive anxiety, anti-social behavior, sleep disorders and weak sensory-motor coordination in the chimera under examination. These are all the typical signs of the patients of schizophrenia.
The study found out that certain genetic dispositions can lead to disease in the progenitor cells that harms the maturation of the glial cells. This, in turn, impairs the formation of myelin by the oligodendrocytes. Consequently, a person develops the chances of being schizophrenic.
In a nutshell, varied decisive genes lead to the defects in the progenitor cells, which trigger the entire impairing process. The research indicated that this might as well be the primary step in the development of treatment drugs to cure schizophrenia. There is also a suggestion of curative chance that can be taken by attempting to replace the defective brain support cells with healthy glial cells.