Adenosine Kinase Expression in the Frontal Cortex in Schizophrenia

Area of Science:

• Neuroscience
• Psychiatry
• Molecular Biology

Background:

• Schizophrenia is linked to adenosine system dysfunction.
• Adenosine kinase (ADK) overexpression is hypothesized to cause this dysfunction.
• Previous studies on ADK expression in schizophrenia are lacking.

Purpose of the Study:

• To investigate ADK gene and protein expression in the brains of schizophrenia patients.
• To examine the effect of antipsychotic treatment on ADK expression in an animal model.

Main Methods:

• Assayed ADK gene and protein expression in dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) from schizophrenia subjects and controls.
• Measured ADK splice variant expression in rat frontal cortex after chronic haloperidol-decanoate treatment.

Main Results:

• No significant differences in ADK-long and -short splice variant expression were found in the DLPFC of schizophrenia patients compared to controls.
• ADK splice variant expression in rats treated with haloperidol-decanoate did not differ significantly.
• ADK protein expression was not significantly altered in the DLPFC or ACC of schizophrenia patients.
• Antipsychotic medication did not significantly affect ADK protein expression in the DLPFC or ACC.

Conclusions:

• Increased ADK expression does not appear to be a significant factor in the hypofunction of the adenosine system in schizophrenia.
• Alternative mechanisms likely underlie adenosine system dysregulation in schizophrenia.