Abstracts from the 28th CINP World Congress of Neuropsychopharmacology, Stockholm, Sweden, 3–7 June 2012

doi:10.1017/s1461145712000508

Cited by 7 publications

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“…Shin et al reported that PTSD patients showed amygdala hyperactivation and frontal hypoactivation and found that these regional activities were significantly correlated with the Clinician-Administered PTSD Scale score [83]. Indeed, some functional magnetic resonance imaging (fMRI) studies have shown an altered resting-state FC in some brain regions, including the amygdala, anterior cingulate cortex (ACC), and medial prefrontal cortex in patients with PTSD, as compared to healthy controls [84,85]. These findings suggest that disrupted frontal network connectivity may be related to those who struggled to recover from adverse experiences [86].…”

Section: The Role Of the Prefrontal Cortex In Cognitive Control Emotmentioning

confidence: 99%

Neurocognitive Mechanism of Human Resilience: A Conceptual Framework and Empirical Review

Yao

Hsieh

2019

IJERPH

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Resilience is an innate human capacity that holds the key to uncovering why some people rebound after trauma and others never recover. Various theories have debated the mechanisms underlying resilience at the psychological level but have not yet incorporated neurocognitive concepts/findings. In this paper, we put forward the idea that cognitive flexibility moderates how well people adapt to adverse experiences, by shifting attention resources between cognition–emotion regulation and pain perception. We begin with a consensus on definitions and highlight the role of cognitive appraisals in mediating this process. Shared concepts among appraisal theories suggest that cognition–emotion, as well as pain perception, are cognitive mechanisms that underlie how people respond to adversity. Frontal brain circuitry sub-serves control of cognition and emotion, connecting the experience of physical pain. This suggests a substantial overlap between these phenomena. Empirical studies from brain imaging support this notion. We end with a discussion of how the role of the frontal brain network in regulating human resilience, including how the frontal brain network interacts with cognition–emotion–pain perception, can account for cognitive theories and why cognitive flexibilities’ role in these processes can create practical applications, analogous to the resilience process, for the recovery of neural plasticity.

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Section: The Role Of the Prefrontal Cortex In Cognitive Control Emotmentioning

confidence: 99%

Neurocognitive Mechanism of Human Resilience: A Conceptual Framework and Empirical Review

Yao

Hsieh

2019

IJERPH

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“…In a two-study series, it was suggested clozapine does not slow grey matter atrophy or loss of white matter integrity in treatment-resistant schizophrenic patients; despite universal clinical improvement (Ahmed et al, 2015;Forde et al, 2012). However, these studies compared treatment-resistant schizophrenic patients on clozapine (n = 33 and n = 21, respectively) to age-matched healthy controls (n = 31 and n = 21, respectively) without a third group of antipsychotic naïve patients or patients on other therapies; making interpretation problematic.…”

Section: Clozapinementioning

confidence: 99%

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Robertson

Coronado

Sethi

et al. 2019

Early Intervention Psych

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Aim: Neuropsychiatric disorders including depression, bipolar and schizophrenia frequently exhibit a neuroprogressive course from prodrome to chronicity. There are a range of agents exhibiting capacity to attenuate biological mechanisms associated with neuroprogression. This review will update the evidence for putative neuroprotective agents including clinical efficacy, mechanisms of action and limitations in current assessment tools, and identify novel agents with neuroprotective potential.Method: Data for this review were sourced from online databases PUBMED, Embase and Web of Science. Only data published since 2012 were included in this review, no data were excluded based on language or publication origin.Results: Each of the agents reviewed inhibit one or multiple pathways of neuroprogression including: inflammatory gene expression and cytokine release, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophin dysregulation and apoptotic signalling. Some demonstrate clinical efficacy in preventing neural damage or loss, relapse or cognitive/functional decline. Agents include: the psychotropic medications lithium, second generation antipsychotics and antidepressants; other pharmacological agents such as minocycline, aspirin, cyclooxygenase-2 inhibitors, statins, ketamine and alpha-2-delta ligands; and others such as erythropoietin, oestrogen, leptin, N-acetylcysteine, curcumin, melatonin and ebselen.Conclusions: Signals of evidence of clinical neuroprotection are evident for a number of candidate agents. Adjunctive use of multiple agents may present a viable avenue to clinical realization of neuroprotection. Definitive prospective studies of neuroprotection with multimodal assessment tools are required.

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Pharmacological interventions for antisocial personality disorder

Khalifa

Gibbon

Völlm

et al. 2020

Cochrane Database of Systematic Reviews

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Abstracts from the 28th CINP World Congress of Neuropsychopharmacology, Stockholm, Sweden, 3–7 June 2012

Cited by 7 publications

References 0 publications

Neurocognitive Mechanism of Human Resilience: A Conceptual Framework and Empirical Review

Neurocognitive Mechanism of Human Resilience: A Conceptual Framework and Empirical Review

Putative neuroprotective pharmacotherapies to target the staged progression of mental illness

Pharmacological interventions for antisocial personality disorder

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