Systematic review, structural analysis, and new theoretical perspectives on the role of serotonin and associated genes in the etiology of psychopathy and sociopathy
Abstract
YILDIRIM, B.O., DERKSEN, J.J.L. Systematic review, structural analysis, and new theoretical perspectives on the role of serotonin and associated genes to the etiology of psychopathy and sociopathy. NEUROSCI BIOBEHAV REV XX(X) XXX-XXX, 2013.- Since its theoretical inception, psychopathy has been considered by philosophers, clinicians, theorists, and empirical researchers to be substantially and critically explained by genetic factors. In this systematic review and structural analysis, new hypotheses will be introduced regarding gene-gene and gene-environment interactions in the etiology of psychopathy and sociopathy. Theory and research from neurobiological and behavioral sciences will be integrated in order to place this work in a broader conceptual framework and promote synergy across fields. First, a between groups comparison between psychopathy and sociopathy is made based on their specific dysfunctions in emotional processing, behavioral profiles, etiological pathways, HPA-axis functioning, and serotonergic profiles. Next, it is examined how various polymorphisms in serotonergic genes (e.g., TPH, 5HTT, HTR1A, HTR2A, HTR2C, and HTR3) might contribute either individually or interactively to the development of these disorders and through which specific biological and behavioral endophenotypes this effect could be mediated. A short introduction is made into mediating variables such as GABAergic functioning and testosterone which could potentially alter the decisive effect of serotonergic genotypes on behavior and physiology. Finally, critical commentary is presented on how to interpret the hypotheses put forward in this review.
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Available from: Bariş O Yildirim, Dec 18, 2013
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- "Thus, with respect to the current results, the observed associations between face processing and psychopathic traits might be the basis for emotion recognition deficits reported in prior studies with criminal offenders. Psychopathy is thought to be associated with changes in the serotonin system (Dolan & Anderson, 2003; Yildirim & Derksen, 2013). Serum serotonin levels were significantly lower in boys with callous-unemotional traits (Moul, Dobson-Stone, Brennan, Hawes, & Dadds, 2013) and several studies have reported an association between antisocial personality disorder and 5-HTTLPR (e.g., Garcia et al., 2010 ). "
[Show abstract] [Hide abstract] ABSTRACT: Deficits in emotional reactivity and recognition have been reported in psychopathy. Impaired attention to the eyes along with amygdala malfunctions may underlie these problems. Here, we investigated how different facets of psychopathy modulate the visual exploration of facial expressions by comparing personality traits in a sample of healthy young adults to eye-tracking data obtained in a face perception task. Fearless Dominance (the interpersonal-emotional facet of psychopathy) and Coldheartedness scores predicted reduced face exploration consistent with findings on lowered emotional reactivity in psychopathy. Moreover, participants high on the social deviance facet of psychopathy ('Self-Centered Impulsivity') showed a reduced bias to shift attention towards the eyes. Our data suggest that facets of psychopathy modulate face processing in healthy individuals and reveal possible attentional mechanisms which might be responsible for the severe impairments of social perception and behavior observed in psychopathy.- "The serotonin system is among the key players in normal affective and cognitive functioning of the brain [1][2][3][4][5] . Better understanding of the complex and multifaceted serotonergic machinery and its specific effects on mood and behavior will help to improve genotyping based risk evaluation and means of pharmaceutical treatment, but hopefully also development of the simple behavioral * Corresponding author. "
[Show abstract] [Hide abstract] ABSTRACT: It is known that 5HTR2A (rs6311) receptors have high concentration in the cortical layer-5 pyramidal neurons and that these receptors play an important role in the modulation of neurocognitive functions. For example, layer-5 pyramidal neurons mediate cellular level integrative interaction of primary sensory afferent signals and top-down signals exerting contextual modulatory influence. It is also known that genetic variability of 5HTR2A is implicated in individual differences in mental processes. Interestingly, serotonin selectively enhances the asynchronous type of glutamate release when modulating the activity of cortical layer-5 pyramidal neurons, with a post-stimulation delay of this effect at about 50 ms. There are not many behavioral tasks capable of tapping that small temporal intervals in terms of change of the values of independent variables leading to an observable change in the subjects’ behavior. However, in the metacontrast masking vision task stimulus onset asynchronies between target and mask critical for the change in the expression of the masking effect correspond to this small temporal value. Thus we hypothesized that genetic variability in 5HTR2A (rs6311) is likely to be associated with different behavioral effects of metacontrast masking and more specifically, that because A allele carriers typically demonstrate greater promoter activity, target-to-mask asynchrony variations should have stronger impact on the masking effect especially with this group of subjects. We obtained support for this hypothesis, but only when target and mask shapes were mutually incongruent.- "Methodological problems, particularly associated with defining and measuring the incidence or timing of adversity or stressful events, may have contributed to variations in the literature (Hammen et al., 2010; Uher and McGuffin, 2008); for example, the influence of 5HTT variants may be particularly potent on childhood adversity as a predisposition for later MDD. It is also apparent that, as for symptoms, this and other serotonin-related genetic variations are not to be associated specifically with one disorder (Yildirim and Derksen, 2013). This would be expected given the widespread action of serotonin on neural and behavioural functions , including reactivity to external events. "
[Show abstract] [Hide abstract] ABSTRACT: Depression (MDD) is prodromal to, and a component of, Alzheimer’s disease (AD): it may also be a trigger for incipient AD. MDD is not a unitary disorder, so there may be particular subtypes of early life MDD that pose independent high risks for later AD, though the identification of these subtypes is problematical. There may either be a common pathological event underlying both MDD and AD, or MDD may sensitize the brain to a second event (‘hit’) that precipitates AD. MDD may also accelerate brain ageing, including altered DNA methylation, increased cortisol but decreasing DHEA and thus the risk for AD. So far, genes predicting AD (e.g. APOEε4) are not risk factors for MDD, and those implicated in MDD (e.g. SLC6A4) are not risks for AD, so a common genetic predisposition looks unlikely. There is as yet no strong indication that an epigenetic event occurs during some forms of MDD that predisposes to later AD, though the evidence is limited.
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