Treatment for Memory Defects Symptomatic of Schizophrenia

News Brief by Rumzah Paracha

         Schizophrenia is a psychiatric disorder that consists of hallucinations and paranoia, which can be treated and controlled with antipsychotic medication, and disruptions in short-term and verbal memory, which have been more difficult to treat. Research has shown that the affects on short term memory are due to stunted growth of neurons and a lack of connections between the hippocampus and pre-frontal cortex.

            Genetic mutation, the 22q11.2 microdeletion, has been identified as the leading genetic risk factor for schizophrenia. Drs. Gogos and Gordon, of the Zuckerman Institute at Columbia University, have discovered that this mutation results in hyper-production of protein Gsk3-beta. Too much Gsk3-beta negatively impacts neuron growth during development. Drs. Gogos and Gordon isolated the 22q11.2 microdeletion in mice and treated them with a chemical compound that blocks Gsk3-beta activity extremely early in their development. This blocking agent prevented Gsl3-beta from stunting neuron growth and the mice did not develop any memory defects characteristic of schizophrenia.

            While this treatment shows great promise, its results have several limitations. The chemical compound was administered early in the mouse’s life but schizophrenia does not manifest until adolescence or early adulthood in humans. Also this is only a potential treatment for the specific cases of schizophrenia that results from the 22q11.2 microdeletion mutation, which is one precent of people with schizophrenia. However, this breakthrough discovery enables scientists to target a specific protein to combat the perviously untreatable aspects of schizophrenia and could be a way to re-establish contact between the hippocampus and pre-frontal cortex, two vital regions of the brain.

 

Original Research:

Makoto Tamura, Jun Mukai, Joshua A. Gordon, Joseph A. Gogos. Developmental Inhibition of Gsk3 Rescues Behavioral and Neurophysiological Deficits in a Mouse Model of Schizophrenia Predisposition. Neuron, 2016 DOI: 10.1016/j.neuron.2016.01.025   

Summarized from:

 The Zuckerman Institute at Columbia University. "Scientists eliminate core symptom of schizophrenia in mice: Team uses chemical compound to restore affected brain regions; findings could lead to new treatment strategies." ScienceDaily. ScienceDaily, 18 February 2016. <www.sciencedaily.com/releases/2016/02/160218132239.htm>.