Schizophrenia is a debilitating mental disease that is characterized by visual or auditory hallucinations and false beliefs known as delusions. Other characteristics include poor speech, loss of interest and neurocognitive deficits that persist for at least six months. With the proper treatment and care, patients with schizophrenia have the potential to live a normal and productive life. Although there is no cure for this disease, symptoms can be managed with antipsychotic medications.
Schizophrenia is a multifactorial disease meaning that there are many causes that contribute to schizophrenia including genetic etiologies and environmental factors. Neurocognitive deficits are commonly seen in individuals with schizophrenia and are characterized by deficits in working memory and executive function such as planning, organizing and the ability to form abstract thoughts. The memory deficits can be chronic depending on the individual.
Reversal of cognitive deficits
A recent article in the Journal of the American Medical Association revealed that the memory deficits caused by a genetic link could be potentially reversed. One of the most common genetic links, called a microdeletion on chromosome 22q11.2, is responsible for the memory loss experienced in individuals with schizophrenia. A microdeletion is a small deletion in the amino acids which make up the proteins. These proteins are responsible for carrying genetic information on chromosomes. When a gene is altered due to any type of deletion, insertion or substitution, the protein becomes messed up leading to an error in the genetic code.
The microdeletion on chromosome 22q11.2 can be reversed using an antagonist of the glycogen synthase kinase 3 β (Gsk3β) protein. Glycogen synthase kinase is a protein that actively plays a role at the cellular level involved in energy metabolism and neuronal cell development. An inhibitor of this microdeletion was administered to mice during early postnatal development. The results showed a reversal of cognitive deficits in the mice.
Prevention of memory deficits
The correlation between mice and humans and the reversal of memory deficits using this inhibitor is not yet solidified. This inhibitor was introduced to mice during their postnatal period, which is comparative to the prenatal period in humans. Schizophrenia is diagnosed in the adolescent period and the average age of onset is between 23 and 35 years old. Therefore, it is important to determine whether the inhibition of Gsk3β later in life can actually prevent memory deficits. Follow-up studies will be needed to determine whether this memory reversal has potential outside the human womb.
Sovereign Health of California is a leading behavioral health care provider with locations across the United States that treat people with addiction, mental health disorders like schizophrenia, and dual diagnosis. For more information, please call our 24/7 helpline.
About the author
Kristen Fuller, M.D., is a senior staff writer at the Sovereign Health Group and enjoys writing about evidence-based topics in the cutting-edge world of medicine. She is a physician and author, who also teaches, practices medicine in the urgent care setting and contributes to medicine board education. She is also an outdoor and dog enthusiast. For more information and other inquiries about this article, contact the author at firstname.lastname@example.org.