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Related Experiment Videos

Is obsessive-compulsive disorder caused by a second-messenger imbalance?

D Marazziti1, J Perez, G B Cassano

  • 1Department of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, Pisa, Italy.

CNS Spectrums
|September 5, 2006
PubMed
Summary
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Obsessive-compulsive disorder (OCD) may stem from an imbalance between protein kinase C (PKC) and protein kinase A (PKA) pathways. This imbalance, favoring PKC, suggests new therapeutic targets for OCD treatment.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Molecular Biology

Background:

  • Obsessive-compulsive disorder (OCD) is a common psychiatric condition with an unknown etiology.
  • Existing research suggests the involvement of the serotonin (5-HT) transporter in OCD.
  • Studies indicate reduced platelet 5-HT transporter functionality in OCD patients.

Purpose of the Study:

  • To investigate the roles of protein kinase C (PKC) and protein kinase A (PKA) in OCD.
  • To propose a unifying hypothesis for the underlying molecular mechanisms of OCD.

Main Methods:

  • Combined data from two independent studies of OCD patients.
  • Assessed the activity levels of PKC and PKA in patient samples.

Main Results:

Related Experiment Videos

  • Observed increased activity of protein kinase C (PKC) in OCD patients.
  • Observed decreased activity of protein kinase A (PKA) in OCD patients.

Conclusions:

  • Hypothesize that OCD may result from an imbalance between PKC and PKA signaling pathways.
  • Suggests a prevalence of the phosphoinositide pathway over the cyclic adenosine monophosphate (cAMP) pathway in OCD.
  • This hypothesis opens avenues for novel therapeutic interventions for OCD.