The Psychobiology of Resilience

CNS Spectrums ◽  
2009 ◽  
Vol 14 (S3) ◽  
pp. 41-47 ◽  
Author(s):  
Dan J. Stein

AbstractAlthough adverse environments are well known to be a risk factor for psychopathology, many individuals respond adaptively to such environments. There is growing interest in the underlying mechanisms involved in such resilience. Several cognitive-affective processes may be involved, and these may be mediated by particular neuronal circuits and neurochemical systems. This article summarizes some of the relevant work on the role of fear conditioning, reward processing, and social behavior in resilience. There is a growing body of data on how particular gene-environment interactions affect these processes, and thus underpin resilience. Ultimately, a better understanding of the mechanisms underpinning resilience may lead to novel interventions.

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Christine Quach ◽  
Ying Song ◽  
Hongrui Guo ◽  
Shun Li ◽  
Hadi Maazi ◽  
...  

AbstractAberrant autophagy is a major risk factor for inflammatory diseases and cancer. However, the genetic basis and underlying mechanisms are less established. UVRAG is a tumor suppressor candidate involved in autophagy, which is truncated in cancers by a frameshift (FS) mutation and expressed as a shortened UVRAGFS. To investigate the role of UVRAGFS in vivo, we generated mutant mice that inducibly express UVRAGFS (iUVRAGFS). These mice are normal in basal autophagy but deficient in starvation- and LPS-induced autophagy by disruption of the UVRAG-autophagy complex. iUVRAGFS mice display increased inflammatory response in sepsis, intestinal colitis, and colitis-associated cancer development through NLRP3-inflammasome hyperactivation. Moreover, iUVRAGFS mice show enhanced spontaneous tumorigenesis related to age-related autophagy suppression, resultant β-catenin stabilization, and centrosome amplification. Thus, UVRAG is a crucial autophagy regulator in vivo, and autophagy promotion may help prevent/treat inflammatory disease and cancer in susceptible individuals.


2016 ◽  
Vol 2016 ◽  
pp. 1-23 ◽  
Author(s):  
Paula Moran ◽  
Jennifer Stokes ◽  
Julia Marr ◽  
Gavin Bock ◽  
Lieve Desbonnet ◽  
...  

The study of gene × environment, as well as epistatic interactions in schizophrenia, has provided important insight into the complex etiopathologic basis of schizophrenia. It has also increased our understanding of the role of susceptibility genes in the disorder and is an important consideration as we seek to translate genetic advances into novel antipsychotic treatment targets. This review summarises data arising from research involving the modelling of gene × environment interactions in schizophrenia using preclinical genetic models. Evidence for synergistic effects on the expression of schizophrenia-relevant endophenotypes will be discussed. It is proposed that valid and multifactorial preclinical models are important tools for identifying critical areas, as well as underlying mechanisms, of convergence of genetic and environmental risk factors, and their interaction in schizophrenia.


2021 ◽  
pp. 469-474
Author(s):  
M KNÍŽE ◽  
J PIŤHA ◽  
J HUBACEK ◽  
T FAIT

Among unique cardiovascular risk factors in women are complications during pregnancy, including miscarriage. Important risk factor is also genetic background. One of powerful candidate genes for cardiovascular disease of atherosclerotic origin (aCVD) is gene for connexin 37 (Cx37) with strong gene-environment interaction including smoking status, that is also strong risk factor for complications in pregnancy including spontaneous abortion (SA). We analyzed association between SA and Cx37 gene polymorphism (1019C>T; Pro319Ser) in 547 fetuses and its potential interaction with smoking status of mothers. Using genetic analyses from women from general population as controls, ORs for T allele, found in our previous studies to be protective against aCVD, were calculated. T allele carriers (fetuses), had OR 0.91 (95 % CI 0.72-1.14) and no interaction with smoking was observed. In conclusion, no significant association between Cx37 polymorphism and SA was observed and no modifying effect of smoking status on this association was detected.


Author(s):  
Lane Beckes ◽  
Weston Layne Edwards

This chapter provides an overview and novel theoretical synthesis of the literature on how and why emotions regulate social behaviors. It outlines how theorists in this domain have long disagreed on how to conceptualize the role of evolution and innateness in terms of functions of emotions. Parsing theoretical and empirical traditions by level of domain specificity, the chapter argues for a domain-relevant approach to emotion, which is more congruent with current understanding of neurodevelopment and gene–environment interactions. It examines emotion as emergent information about the motivational landscape and offers an alternative metaphorical approach to thinking about evolution as it relates to socioemotional life based on river formation and change.


Author(s):  
Anna Maria Gori ◽  
Francesco Sofi ◽  
Rossella Marcucci ◽  
Betti Giusti ◽  
Gian Franco Gensini ◽  
...  

AbstractDuring the last years, a growing body of evidence has been accumulated on the role of hyperhomocysteinemia in the occurrence of coronary artery disease and other arterial occlusive diseases. The mechanism by which high circulating homocysteine concentrations are a risk factor for atherothrombosis is incompletely understood. The present review is aimed to evaluate the role of inflammation in influencing homocysteine (Hcy) and vitamin BClin Chem Lab Med 2007;45:1728–36.


2011 ◽  
Vol 26 (S2) ◽  
pp. 1980-1980
Author(s):  
A. Staniloiu ◽  
H.J. Markowitsch

IntroductionThe prediction, prevention and treatment of violence pose several challenges that are partly due to incompletely described neurobiological underpinnings of human violent behavior.ObjectivesThis work's objectives are establishing greater recognition of the neurochemical substrates of violent behavior and importance of the gene-environment interplay in the development of violence, distinguishing the components of the functional neural networks involved in violent behavior and facilitating the interpretation of relations between brain damage and alterations in social behavior from a perspective that takes into account variables such as developmental phase, brain-environment interactions and neuroplasticity.AimsWe provide an overview of the neurobiological underpinnings of violence and the roles and advantages of using static and functional brain imaging in studying violent behavior.MethodsA comprehensive review of the scientific literature on the neurobiology of violence was performed. A theoretical framework for the possible role of epigenetic factors in mediating the predisposition for violence is advanced.ResultsResearch data from various fields (such as genetics, cognitive and affective neurosciences, static and functional neuroimaging) suggest that the predisposition for violent behavior is influenced by both genetic and environmental factors. Epigenetic mechanisms underlying lasting environmentally-induced modifications in gene expression have recently been implicated in the pathogeny of various psychiatric and non-psychiatric diseases and social behavior disturbances.ConclusionsThe genetic, neurochemical and neuroimaging findings from various studies emphasize the complex role of the gene-environment interplay in the pathogenesis of violence and open a path of hope for the development and optimal timing of violence prevention strategies.


2008 ◽  
Vol 24 (4) ◽  
pp. 218-225 ◽  
Author(s):  
Bertram Gawronski ◽  
Roland Deutsch ◽  
Etienne P. LeBel ◽  
Kurt R. Peters

Over the last decade, implicit measures of mental associations (e.g., Implicit Association Test, sequential priming) have become increasingly popular in many areas of psychological research. Even though successful applications provide preliminary support for the validity of these measures, their underlying mechanisms are still controversial. The present article addresses the role of a particular mechanism that is hypothesized to mediate the influence of activated associations on task performance in many implicit measures: response interference (RI). Based on a review of relevant evidence, we argue that RI effects in implicit measures depend on participants’ attention to association-relevant stimulus features, which in turn can influence the reliability and the construct validity of these measures. Drawing on a moderated-mediation model (MMM) of task performance in RI paradigms, we provide several suggestions on how to address these problems in research using implicit measures.


2015 ◽  
Vol 27 (4) ◽  
pp. 159-169 ◽  
Author(s):  
Elsbeth D. Asbeek Brusse ◽  
Marieke L. Fransen ◽  
Edith G. Smit

Abstract. This study examined the effects of disclosure messages in entertainment-education (E-E) on attitudes toward hearing protection and attitude toward the source. In addition, the (mediating) role of the underlying mechanisms (i.e., transportation, identification, and counterarguing) was studied. In an experiment (N = 336), three different disclosure messages were compared with a no-disclosure condition. The results show that more explicit disclosure messages negatively affect transportation and identification and stimulate the generation of counterarguments. In addition, the more explicit disclosure messages affect both attitude measures via two of these processes (i.e., transportation and counterarguing). Less explicit disclosure messages do not have this effect. Implications of the findings are discussed.


2017 ◽  
Vol 225 (3) ◽  
pp. 200-213 ◽  
Author(s):  
Christian Baumann ◽  
Miriam A. Schiele ◽  
Martin J. Herrmann ◽  
Tina B. Lonsdorf ◽  
Peter Zwanzger ◽  
...  

Abstract. Conditioning and generalization of fear are assumed to play central roles in the pathogenesis of anxiety disorders. Here we investigate the influence of a psychometric anxiety-specific factor on these two processes, thus try to identify a potential risk factor for the development of anxiety disorders. To this end, 126 healthy participants were examined with questionnaires assessing symptoms of anxiety and depression and with a fear conditioning and generalization paradigm. A principal component analysis of the questionnaire data identified two factors representing the constructs anxiety and depression. Variations in fear conditioning and fear generalization were solely associated with the anxiety factor characterized by anxiety sensitivity and agoraphobic cognitions; high-anxious individuals exhibited stronger fear responses (arousal) during conditioning and stronger generalization effects for valence and UCS-expectancy ratings. Thus, the revealed psychometric factor “anxiety” was associated with enhanced fear generalization, an assumed risk factor for anxiety disorders. These results ask for replication with a longitudinal design allowing to examine their predictive validity.


2017 ◽  
Vol 225 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Tina B. Lonsdorf ◽  
Jan Richter

Abstract. As the criticism of the definition of the phenotype (i.e., clinical diagnosis) represents the major focus of the Research Domain Criteria (RDoC) initiative, it is somewhat surprising that discussions have not yet focused more on specific conceptual and procedural considerations of the suggested RDoC constructs, sub-constructs, and associated paradigms. We argue that we need more precise thinking as well as a conceptual and methodological discussion of RDoC domains and constructs, their interrelationships as well as their experimental operationalization and nomenclature. The present work is intended to start such a debate using fear conditioning as an example. Thereby, we aim to provide thought-provoking impulses on the role of fear conditioning in the age of RDoC as well as conceptual and methodological considerations and suggestions to guide RDoC-based fear conditioning research in the future.


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