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Developing a Rat Model for Bipolar Disorder
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Akt-mTOR hypoactivity in bipolar disorder gives rise to cognitive impairments associated with altered neuronal

Amanda M Vanderplow1, Andrew L Eagle2, Bailey A Kermath1

  • 1Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.

Neuron
|March 25, 2021
PubMed

Insights

Reduced Akt-mammalian target of rapamycin (mTOR) pathway signaling in the prefrontal cortex (PFC) is linked to bipolar disorder. Akt hypofunction in the PFC can cause cognitive deficits and alter synaptic function.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Akt-family kinases are implicated in schizophrenia and bipolar disorder.
  • Prefrontal cortex (PFC) dysfunction is central to these disorders.
  • Akt-mammalian target of rapamycin (mTOR) pathway alterations in the PFC remain understudied in bipolar disorder and schizophrenia.

Purpose of the Study:

  • To investigate Akt-mTOR pathway activity and protein expression in the PFC of individuals with bipolar disorder and schizophrenia.
  • To explore the functional consequences of reduced Akt signaling in the PFC.

Main Methods:

  • Analysis of key Akt-mTOR pathway proteins in postmortem PFC homogenates from bipolar disorder and schizophrenia subjects.
  • Utilizing a reverse-translational approach to model Akt hypofunction in the PFC.

Main Results:

  • Identified reduced Akt-mTOR signaling in the PFC of a subset of bipolar disorder patients.
  • Demonstrated that Akt hypofunction in the PFC can induce cognitive phenotypes.
  • Observed associated alterations in synaptic connectivity and function due to Akt hypofunction.

Conclusions:

  • Akt-mTOR pathway dysregulation in the PFC may contribute to the pathophysiology of bipolar disorder.
  • PFC Akt hypofunction is sufficient to model key cognitive and synaptic deficits observed in psychiatric disorders.
Keywords:
aktautophagybipolar disordercognitiondendritic spinemTORmemoryprefrontal cortexsynapseulk1

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