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Crosstalk between 5-HT2cR and PTEN signaling pathway in atypical antipsychotic-induced metabolic syndrome and

Jun Cai1, Zhenghui Yi, Weihong Lu

  • 1Schizophrenia Program, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China.

Medical Hypotheses
|February 5, 2013
PubMed

Insights

Atypical antipsychotics (AAPs) may cause metabolic syndrome and cognitive issues by disrupting the 5-HT2c receptor (5-HT2cR) pathway. This disruption affects signaling crucial for both metabolic health and brain function.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Metabolic Disorders

Background:

  • Atypical antipsychotics (AAPs) are linked to metabolic syndrome (MetS) and cognitive dysfunction.
  • Patients with MetS on antipsychotic treatment show worse cognitive function, suggesting a link between MetS and cognition.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying AAP-induced MetS and cognitive impairments.
  • To explore the role of the 5-HT2c receptor (5-HT2cR) and its interaction with PTEN in these side effects.

Main Methods:

  • The study proposes a hypothesis based on existing evidence of crosstalk between 5-HT2cR and PTEN.
  • It focuses on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, which is regulated by PTEN.

Main Results:

  • 5-HT2cR antagonism by AAPs may disrupt the 5-HT2cR-PTEN crosstalk.
  • This disruption could lead to aberrant PI3K/AKT signaling in both peripheral tissues and the central nervous system.

Conclusions:

  • AAP-induced MetS and cognitive deficits may arise from a common pathway involving disrupted 5-HT2cR-PTEN signaling.
  • Targeting this pathway could offer strategies to mitigate AAPs' adverse effects.

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