Serotonin and impulsive aggression

Coccaro, Emil F.; Fanning, Jennifer R.; Phan, K. Luan; Lee, Royce

doi:10.1017/s1092852915000310

Cited by 130 publications

(113 citation statements)

References 67 publications

(95 reference statements)

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“…On the molecular level, serotonergic (Coccaro et al, 2015), neuropeptide (Coccaro et al, 1998), and inflammatory protein abnormalities have been linked to impulsive aggression. At the macro level, functional brain imaging studies have found evidence of exaggerated amygdala response to angry faces and diminished functional connectivity between the amygdala and orbitofrontal cortex (Coccaro et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

White Matter Integrity Reductions in Intermittent Explosive Disorder

Lee

Arfanakis

Evia

et al. 2016

Neuropsychopharmacol

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Intermittent explosive disorder (IED), as described in DSM-5, is the categorical expression of pathological impulsive aggression. Previous work has identified neurobiological correlates of the disorder in patterns of frontal-limbic brain activity and dysregulation of serotonergic neurotransmission. Given the importance of short-and-long range white matter connections of the brain in social and emotional behavior, studies of white matter connectivity in impulsive aggression are warranted. Diffusion tensor imaging (DTI) studies in the related conditions of antisocial and borderline personality disorder have produced preliminary evidence of disturbed white matter connectivity in these disorders, but to date there have been no DTI studies in IED. A total of 132 male and female adults between the ages of 18 and 55 years underwent Turboprop-DTI on a 3-Tesla MRI scanner. Of these, 42 subjects had IED, 40 were normal controls, and 50 were clinical psychiatric controls with psychiatric disorders without IED. All subjects were free of alcohol, psychotropic medications, or drugs of abuse. The diffusion tensor was calculated in each voxel and maps of fractional anisotropy (FA) were generated. Tract-based spatial statistics (TBSS) were used to compare FA along the white matter skeleton among the three subject groups. IED was associated with lower FA in two clusters located in the superior longitudinal fasciculus (SLF) when compared with the psychiatric and healthy controls. Impulsive aggression and borderline personality disorder, but not psychopathy or antisocial personality disorder, was associated with lower FA in the two clusters within the SLF. In conclusion, IED was associated with lower white matter integrity in long-range connections between the frontal and temporoparietal regions.

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Section: Introductionmentioning

confidence: 99%

White Matter Integrity Reductions in Intermittent Explosive Disorder

Lee

Arfanakis

Evia

et al. 2016

Neuropsychopharmacol

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Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 99%

“…Among the various neurochemical pathways putatively involved, the serotonin (5-hydoxytryptamine [5-HT]) system has been the focus of extensive investigations [13,14]. A parsimonious mechanistic neurobiological model linking the 5-HT system with aggression points to behavioral inhibition as a key mediator [14]. According to this model, a greater activity of the 5-HT system would correspond to a greater behavioral inhibition of the aggressive individual when confronted with threat or frustration [14].…”

Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 99%

“…A parsimonious mechanistic neurobiological model linking the 5-HT system with aggression points to behavioral inhibition as a key mediator [14]. According to this model, a greater activity of the 5-HT system would correspond to a greater behavioral inhibition of the aggressive individual when confronted with threat or frustration [14]. Thus, several elements of the serotonergic system, such as 5-HT peripheral or cerebrospinal fluid levels, 5-HT receptors, metabolic enzymes and their encoding genes, have been tested as plausible biomarkers of aggression [13].…”

Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 99%

“…Aggressive/violent behavior is heterogeneous in its phenotypic manifestation as well as in its origin. From a phenomenological point of view, aggression can be classified as impulsive or premeditated/instrumental [14,16]. Typically, impulsive aggression is enacted in response to a threat or a provocation, while premeditated/instrumental aggressions are committed with the purpose of gaining something [16].…”

Section: Neurobiological Basis Of Aggressive/violent Behavior: Insighmentioning

confidence: 99%

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Preventing Aggressive/Violent Behavior: A Role for Biomarkers?

Pinna

Manchia

2017

Biomark. Med.

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The burden of aggressive/violent behavior Despite a declining rate in the past 10 years, aggressive/violent behavior remains among the main causes of worldwide premature mortality [1]. Associated direct (medical and nonmedical expenditure) and indirect (longterm societal implications) socio-economic costs are also substantial [2,3]. These have been estimated in 2001 at approximately 5% of the gross national product of industrialized countries, and as much as 14% of the gross national product of low-income countries [3].In this context, policy makers have attempted to enact interventions that could prevent the development of aggression and violence in at-risk populations (i.e., abused children and troubled youth, alcohol and substance abusers, prisoners). These public health approaches that include, among the others, education, behavior change, policy, engineering and environmental support, have proven to be effective in reducing the rates of aggression/violence as well as its associated economic costs [4].Nonetheless, there is still a substantial proportion of individuals who enact aggressive/violent behavior over the lifetime course that is not targeted by these interventions. Further, such interventions are implemented only once aggressive behavior has already manifested itself.By definition, primary preventive strategies intend to avoid the manifestation of a specific disease or event before it occurs. To be effective, preventive approaches need to identify risk factors that can determine the onset of an illness or of an event in an exposed population.In the case of aggressive/violent behavior, there is a multitude of determinants (clinical, environmental and biological) that set the liability threshold for its manifestation. It is plausible that predictive models integrating different levels of information (from phenotypic to 'omics' data) might help identifying with higher accuracy individuals at risk for aggression/violence compared with those relying only, for instance, on clinical data. However, the inclusion of biological markers (henceforth biomarkers) in such models can be achieved only if they are identified in longitudinal prospective studies and are replicated in independent samples. Importantly, this process could also lead to a more precise understanding of the neurobiological underpinnings of aggression/violence.Here, we critically discuss the recent advancements in the identification of biological markers of aggression and the eventual barriers toward their implementation in predictive models. To this end, we will first briefly present the current knowledge on the neurobiological make up of aggression/violent behavior. Next, we will discuss how the phenotypic heterogeneity of aggression might have hindered the identification of reliable biomarkers. Finally, we will present data on available biological markers of aggression that might be suitable for implementation in predictive models.

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