Akt-mTOR hypoactivity in bipolar disorder gives rise to cognitive impairments associated with altered neuronal structure and function
The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although...
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| Published in | Neuron (Cambridge, Mass.) Vol. 109; no. 9; pp. 1479 - 1496.e6 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
05.05.2021
Elsevier Limited |
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| Abstract | The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function.
•A reduction in Akt-mTOR signaling occurs in the PFC of male bipolar disorder subjects•Akt hypofunction reduces synaptic structural and functional plasticity in the PFC•Akt hypofunction is sufficient to impair PFC-mediated cognition
The biochemical changes that contribute to bipolar disorder pathophysiology remain largely unknown. Cahill et al. reveal a reduction in the activation of the Akt-mTOR pathway in the prefrontal cortex of bipolar disorder subjects. Cahill et al. demonstrate that reduced activity of this pathway causes cognitive and synaptic phenotypes. |
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| AbstractList | The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function.The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function. SummaryThe Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function. The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function. •A reduction in Akt-mTOR signaling occurs in the PFC of male bipolar disorder subjects•Akt hypofunction reduces synaptic structural and functional plasticity in the PFC•Akt hypofunction is sufficient to impair PFC-mediated cognition The biochemical changes that contribute to bipolar disorder pathophysiology remain largely unknown. Cahill et al. reveal a reduction in the activation of the Akt-mTOR pathway in the prefrontal cortex of bipolar disorder subjects. Cahill et al. demonstrate that reduced activity of this pathway causes cognitive and synaptic phenotypes. The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified Akt-family kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction in the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function. The Akt family of kinases exert many of their cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of intermediary proteins. Multiple lines of evidence have identified the Akt family of kinases as candidate schizophrenia and bipolar disorder genes. Although dysfunction of the prefrontal cortex (PFC) is a key feature of both schizophrenia and bipolar disorder, no studies have comprehensively assessed potential alterations in Akt-mTOR pathway activity in the PFC of either disorder. Here, we examined the activity and expression profile of key proteins in the Akt-mTOR pathway in bipolar disorder and schizophrenia homogenates from two different PFC subregions. Our findings identify reduced Akt-mTOR PFC signaling in a subset of bipolar disorder subjects. Using a reverse-translational approach, we demonstrated that Akt hypofunction the PFC is sufficient to give rise to key cognitive phenotypes that are paralleled by alterations in synaptic connectivity and function. The biochemical changes that contribute to bipolar disorder pathophysiology remain largely unknown. Cahill et al. reveal a reduction in the activation of the Akt-mTOR pathway in the prefrontal cortex of bipolar disorder subjects. Cahill et al. demonstrate that reduced activity of this pathway causes cognitive and synaptic phenotypes. |
| Author | Kermath, Bailey A. Cahill, Michael E. Bjornson, Kathryn J. Vanderplow, Amanda M. Eagle, Andrew L. Robison, Alfred J. |
| AuthorAffiliation | 3 Lead contact 1 Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI, 53706 USA 2 Department of Physiology, Michigan State University, East Lansing, MI, 48824 USA |
| AuthorAffiliation_xml | – name: 2 Department of Physiology, Michigan State University, East Lansing, MI, 48824 USA – name: 1 Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI, 53706 USA – name: 3 Lead contact |
| Author_xml | – sequence: 1 givenname: Amanda M. surname: Vanderplow fullname: Vanderplow, Amanda M. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA – sequence: 2 givenname: Andrew L. surname: Eagle fullname: Eagle, Andrew L. organization: Department of Physiology, Michigan State University, East Lansing, MI 48824, USA – sequence: 3 givenname: Bailey A. surname: Kermath fullname: Kermath, Bailey A. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA – sequence: 4 givenname: Kathryn J. surname: Bjornson fullname: Bjornson, Kathryn J. organization: Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA – sequence: 5 givenname: Alfred J. surname: Robison fullname: Robison, Alfred J. organization: Department of Physiology, Michigan State University, East Lansing, MI 48824, USA – sequence: 6 givenname: Michael E. surname: Cahill fullname: Cahill, Michael E. email: michael.cahill@wisc.edu organization: Department of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33765445$$D View this record in MEDLINE/PubMed |
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| Keywords | bipolar disorder memory autophagy cognition prefrontal cortex mTOR dendritic spine akt synapse ulk1 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Author Contributions Behavioral experiments were performed by A.M.V., B.A.K., and M.E.C. Biochemistry experiments and analyses were performed by A.M.V., B.A.K., K.J.B., and M.E.C. Electrophysiology experiments were performed by A.L.E. and A.J.R. Dendritic spine imaging and analysis was performed by A.M.V. and M.E.C. A.M.V. and M.E.C. wrote the paper. |
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| Snippet | The Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of... SummaryThe Akt family of kinases exerts many of its cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of... The Akt family of kinases exert many of their cellular effects via the activation of the mammalian target of rapamycin (mTOR) kinase through a series of... |
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| SubjectTerms | akt AKT protein autophagy Bipolar disorder Bipolar Disorder - metabolism Bipolar Disorder - pathology Bipolar Disorder - physiopathology cognition Cognitive ability Cognitive Dysfunction - metabolism Cognitive Dysfunction - pathology Cognitive Dysfunction - physiopathology Consortia dendritic spine Female Genes Genomics Humans Kinases Male memory Mental disorders mTOR Neural networks Neurons - pathology Phenotypes Phosphorylation Prefrontal cortex Prefrontal Cortex - metabolism Prefrontal Cortex - pathology Prefrontal Cortex - physiopathology Proteins Proto-Oncogene Proteins c-akt - metabolism Psychosis Rapamycin Schizophrenia Structure-function relationships synapse TOR protein TOR Serine-Threonine Kinases - metabolism ulk1 |
| Title | Akt-mTOR hypoactivity in bipolar disorder gives rise to cognitive impairments associated with altered neuronal structure and function |
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