Animal models to improve our understanding and treatment of suicidal behavior

TD Gould; P Georgiou; LA Brenner; L Brundin; A Can; P Courtet; ZR Donaldson; Y Dwivedi; S Guillaume; II Gottesman; S Kanekar; CA Lowry; PF Renshaw; D Rujescu; EG Smith; G Turecki; P Zanos; CA Zarate; PA Zunszain; TT Postolache

doi:10.1038/tp.2017.50

Animal models to improve our understanding and treatment of suicidal behavior

TD Gould, P Georgiou, LA Brenner, L Brundin, A Can, P Courtet, ZR Donaldson, Y Dwivedi, S Guillaume, II Gottesman, S Kanekar, CA Lowry, PF Renshaw, D Rujescu, EG Smith, G Turecki, P Zanos, CA Zarate, PA Zunszain, TT Postolache

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Abstract

Worldwide, suicide is a leading cause of death. Although a sizable proportion of deaths by suicide may be preventable, it is well documented that despite major governmental and international investments in research, education and clinical practice suicide rates have not diminished and are even increasing among several at-risk populations. Although nonhuman animals do not engage in suicidal behavior amenable to translational studies, we argue that animal model systems are necessary to investigate candidate endophenotypes of suicidal behavior and the neurobiology underlying these endophenotypes. Animal models are similarly a critical resource to help delineate treatment targets and pharmacological means to improve our ability to manage the risk of suicide. In particular, certain pathophysiological pathways to suicidal behavior, including stress and hypothalamic-pituitary-adrenal axis dysfunction, neurotransmitter system abnormalities, endocrine and neuroimmune changes, aggression, impulsivity and decision-making deficits, as well as the role of critical interactions between genetic and epigenetic factors, development and environmental risk factors can be modeled in laboratory animals. We broadly describe human biological findings, as well as protective effects of medications such as lithium, clozapine, and ketamine associated with modifying risk of engaging in suicidal behavior that are readily translatable to animal models. Endophenotypes of suicidal behavior, studied in animal models, are further useful for moving observed associations with harmful environmental factors (for example, childhood adversity, mechanical trauma aeroallergens, pathogens, inflammation triggers) from association to causation, and developing preventative strategies. Further study in animals will contribute to a more informed, comprehensive, accelerated and ultimately impactful suicide research portfolio

Original language	English
Article number	e1092
Pages (from-to)	1-22
Journal	Translational psychiatry
Volume	7
DOIs	https://doi.org/10.1038/tp.2017.50
Publication status	Published - 11 Apr 2017

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Animal models to improve our_GOULD_Accepted 1February 2017_Online 11April2017 GOLD VoR CCBYFinal published version, 971 KBLicence: CC BY

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Gould, TD., Georgiou, P., Brenner, LA., Brundin, L., Can, A., Courtet, P., Donaldson, ZR., Dwivedi, Y., Guillaume, S., Gottesman, II., Kanekar, S., Lowry, CA., Renshaw, PF., Rujescu, D., Smith, EG., Turecki, G., Zanos, P., Zarate, CA., Zunszain, PA., & Postolache, TT. (2017). Animal models to improve our understanding and treatment of suicidal behavior. Translational psychiatry, 7, 1-22. Article e1092. https://doi.org/10.1038/tp.2017.50

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abstract = "Worldwide, suicide is a leading cause of death. Although a sizable proportion of deaths by suicide may be preventable, it is well documented that despite major governmental and international investments in research, education and clinical practice suicide rates have not diminished and are even increasing among several at-risk populations. Although nonhuman animals do not engage in suicidal behavior amenable to translational studies, we argue that animal model systems are necessary to investigate candidate endophenotypes of suicidal behavior and the neurobiology underlying these endophenotypes. Animal models are similarly a critical resource to help delineate treatment targets and pharmacological means to improve our ability to manage the risk of suicide. In particular, certain pathophysiological pathways to suicidal behavior, including stress and hypothalamic-pituitary-adrenal axis dysfunction, neurotransmitter system abnormalities, endocrine and neuroimmune changes, aggression, impulsivity and decision-making deficits, as well as the role of critical interactions between genetic and epigenetic factors, development and environmental risk factors can be modeled in laboratory animals. We broadly describe human biological findings, as well as protective effects of medications such as lithium, clozapine, and ketamine associated with modifying risk of engaging in suicidal behavior that are readily translatable to animal models. Endophenotypes of suicidal behavior, studied in animal models, are further useful for moving observed associations with harmful environmental factors (for example, childhood adversity, mechanical trauma aeroallergens, pathogens, inflammation triggers) from association to causation, and developing preventative strategies. Further study in animals will contribute to a more informed, comprehensive, accelerated and ultimately impactful suicide research portfolio",

author = "TD Gould and P Georgiou and LA Brenner and L Brundin and A Can and P Courtet and ZR Donaldson and Y Dwivedi and S Guillaume and II Gottesman and S Kanekar and CA Lowry and PF Renshaw and D Rujescu and EG Smith and G Turecki and P Zanos and CA Zarate and PA Zunszain and TT Postolache",

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Gould, TD, Georgiou, P, Brenner, LA, Brundin, L, Can, A, Courtet, P, Donaldson, ZR, Dwivedi, Y, Guillaume, S, Gottesman, II, Kanekar, S, Lowry, CA, Renshaw, PF, Rujescu, D, Smith, EG, Turecki, G, Zanos, P, Zarate, CA, Zunszain, PA & Postolache, TT 2017, 'Animal models to improve our understanding and treatment of suicidal behavior', Translational psychiatry, vol. 7, e1092, pp. 1-22. https://doi.org/10.1038/tp.2017.50

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T1 - Animal models to improve our understanding and treatment of suicidal behavior

AU - Gould, TD

AU - Georgiou, P

AU - Brenner, LA

AU - Brundin, L

AU - Can, A

AU - Courtet, P

AU - Donaldson, ZR

AU - Dwivedi, Y

AU - Guillaume, S

AU - Gottesman, II

AU - Kanekar, S

AU - Lowry, CA

AU - Renshaw, PF

AU - Rujescu, D

AU - Smith, EG

AU - Turecki, G

AU - Zanos, P

AU - Zarate, CA

AU - Zunszain, PA

AU - Postolache, TT

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N2 - Worldwide, suicide is a leading cause of death. Although a sizable proportion of deaths by suicide may be preventable, it is well documented that despite major governmental and international investments in research, education and clinical practice suicide rates have not diminished and are even increasing among several at-risk populations. Although nonhuman animals do not engage in suicidal behavior amenable to translational studies, we argue that animal model systems are necessary to investigate candidate endophenotypes of suicidal behavior and the neurobiology underlying these endophenotypes. Animal models are similarly a critical resource to help delineate treatment targets and pharmacological means to improve our ability to manage the risk of suicide. In particular, certain pathophysiological pathways to suicidal behavior, including stress and hypothalamic-pituitary-adrenal axis dysfunction, neurotransmitter system abnormalities, endocrine and neuroimmune changes, aggression, impulsivity and decision-making deficits, as well as the role of critical interactions between genetic and epigenetic factors, development and environmental risk factors can be modeled in laboratory animals. We broadly describe human biological findings, as well as protective effects of medications such as lithium, clozapine, and ketamine associated with modifying risk of engaging in suicidal behavior that are readily translatable to animal models. Endophenotypes of suicidal behavior, studied in animal models, are further useful for moving observed associations with harmful environmental factors (for example, childhood adversity, mechanical trauma aeroallergens, pathogens, inflammation triggers) from association to causation, and developing preventative strategies. Further study in animals will contribute to a more informed, comprehensive, accelerated and ultimately impactful suicide research portfolio

AB - Worldwide, suicide is a leading cause of death. Although a sizable proportion of deaths by suicide may be preventable, it is well documented that despite major governmental and international investments in research, education and clinical practice suicide rates have not diminished and are even increasing among several at-risk populations. Although nonhuman animals do not engage in suicidal behavior amenable to translational studies, we argue that animal model systems are necessary to investigate candidate endophenotypes of suicidal behavior and the neurobiology underlying these endophenotypes. Animal models are similarly a critical resource to help delineate treatment targets and pharmacological means to improve our ability to manage the risk of suicide. In particular, certain pathophysiological pathways to suicidal behavior, including stress and hypothalamic-pituitary-adrenal axis dysfunction, neurotransmitter system abnormalities, endocrine and neuroimmune changes, aggression, impulsivity and decision-making deficits, as well as the role of critical interactions between genetic and epigenetic factors, development and environmental risk factors can be modeled in laboratory animals. We broadly describe human biological findings, as well as protective effects of medications such as lithium, clozapine, and ketamine associated with modifying risk of engaging in suicidal behavior that are readily translatable to animal models. Endophenotypes of suicidal behavior, studied in animal models, are further useful for moving observed associations with harmful environmental factors (for example, childhood adversity, mechanical trauma aeroallergens, pathogens, inflammation triggers) from association to causation, and developing preventative strategies. Further study in animals will contribute to a more informed, comprehensive, accelerated and ultimately impactful suicide research portfolio

U2 - 10.1038/tp.2017.50

DO - 10.1038/tp.2017.50

M3 - Article

SN - 2158-3188

VL - 7

SP - 1

EP - 22

JO - Translational psychiatry

JF - Translational psychiatry

M1 - e1092

ER -

Animal models to improve our understanding and treatment of suicidal behavior

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