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Comment
. 2021 May 18;2(5):100282.
doi: 10.1016/j.xcrm.2021.100282.

PFC mTOR signaling as a biological signature for cognitive deficits in bipolar disorder without psychosis

Jelena Radulovic  1 , Vilma Gabbay  1   2
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Comment

PFC mTOR signaling as a biological signature for cognitive deficits in bipolar disorder without psychosis

Jelena Radulovic et al. Cell Rep Med. .

Abstract

Vanderplow et al.1 report decreased PFC Akt-mTOR signaling in males with bipolar disorder (BD) without psychosis compared with those with psychosis, possibly related to cognitive deficits. Understanding how cognition differs between these BD subtypes clinically and biologically remains a challenge.

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Figure 1
Figure 1
Implication of Akt family of protein kinases in BD without psychosis (A) Decreased levels of phosphorylated (active) forms of multiple components of Akt signaling in human DL and VL PFC. (B) Deficits of short-term episodic-like memory in mice injected with dominant negative Akt in the prelimbic and infralimbic PFC areas. DN-Akt, dominant negative Akt; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; mTOR, p70S6K, p70 S6 kinase. Human and mouse PFC image credit: Allen Institute.
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References

    1. Vanderplow A.M., Eagle A.L., Kermath B.A., Bjornson K.J., Robison A.J., Cahill M.E. Akt-mTOR hypoactivity in bipolar disorder gives rise to cognitive impairments associated with altered neuronal structure and function. Neuron. 2021;2021 doi: 10.1016/j.neuron.2021.03.008. S0896-6273(21)00156-2. - DOI - PMC - PubMed
    1. Costa-Mattioli M., Monteggia L.M. mTOR complexes in neurodevelopmental and neuropsychiatric disorders. Nat. Neurosci. 2013;16:1537–1543. doi: 10.1038/nn.3546. - DOI - PubMed
    1. Abdallah C.G., Averill L.A., Gueorguieva R., Goktas S., Purohit P., Ranganathan M., Sherif M., Ahn K.-H., D’Souza D.C., Rormica R. Modulation of the antidepressant effects of ketamine by the mTORC1 inhibitor rapamycin. Neuropsychopharmacology. 2020;45:990–997. doi: 10.1038/s41386-020-0644-9. - DOI - PMC - PubMed
    1. Abelaira H.M., Réus G.Z., Ignácio Z.M., Dos Santos M.A., de Moura A.B., Matos D., Demo J.P., da Silva J.B., Michels M., Abatti M. Effects of ketamine administration on mTOR and reticulum stress signaling pathways in the brain after the infusion of rapamycin into prefrontal cortex. J. Psychiatr. Res. 2017;87:81–87. doi: 10.1016/j.jpsychires.2016.12.002. - DOI - PubMed
    1. Chalecka-Franaszek E., Chuang D.M. Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons. Proc. Natl. Acad. Sci. USA. 1999;96:8745–8750. doi: 10.1073/pnas.96.15.8745. - DOI - PMC - PubMed

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