Atypical social reward anticipation as a transdiagnostic characteristic of psychopathology: A meta-analytic review and critical evaluation of current evidence

Aldridge-Waddon, Luke; Vanova, Martina; Munneke, Jaap; Puzzo, Ignazio; Kumari, Veena

doi:10.1016/j.cpr.2020.101942

Cited by 89 publications

(9 citation statements)

References 111 publications

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“…However, this may have an impact on stress generation and social thinning and subsequent psychiatric risk. Disrupted reward processing has particularly been implicated in the development of depression 82 , but it is also associated with a number of other disorders including attention deficit hyperactivity disorder, eating disorders and schizophrenia 83 .…”

Section: Reward Processingmentioning

confidence: 99%

“…Below we focus, in particular, on the impact of disrupted social reward processing because, almost by definition, maltreated children are less likely to receive predictable social rewards such as praise and affection from their caregivers 84 . Atypical social reward processing is also relevant to our model because it is associated with altered social behaviour and is a transdiagnostic marker of psychopathology, including depression, bipolar disorder, eating disorders and schizophrenia 83,85 .…”

Section: Reward Processingmentioning

confidence: 99%

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Social thinning and stress generation after childhood maltreatment: a neurocognitive social transactional model of psychiatric vulnerability

McCrory

Foulkes

Viding

2022

The Lancet Psychiatry

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Section: Reward Processingmentioning

confidence: 99%

Section: Reward Processingmentioning

confidence: 99%

Social thinning and stress generation after childhood maltreatment: a neurocognitive social transactional model of psychiatric vulnerability

McCrory

Foulkes

Viding

2022

The Lancet Psychiatry

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“…Taken together, these results suggest that low investigation times are not the result of global behavioral inhibition. Low investigation of a novel social stimulus may represent a number of specific deficits, including faulty recognition of a novel stimulus as familiar, inattention to social stimuli, reduced motivation/reward associated with social stimuli, and/or inability to recognize social novelty, all of which have been reported in humans with ASD (Guillory et al, 2021; Hedger and Chakrabarti, 2021; Aldridge-Waddon et al, 2020; Weigelt et al, 2012; Chevallier et al, 2012). More specifically related to the Shank3B mouse model, individuals diagnosed with both Phelan-McDermid syndrome and ASD exhibit reduced social attention and reduced social novelty recognition under certain conditions (Guillory et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Activation of the CA2-vCA1 pathway reverses social discrimination dysfunction inShank3Bknockout mice

Cope

Wang

Waters

et al. 2022

Preprint

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Social memory dysfunction is a feature of several neuropsychiatric and neurodevelopmental disorders. Mutation or deletion of the SHANK3 gene, which codes for a synaptic scaffolding protein, has been linked to autism spectrum disorder (ASD) and Phelan-McDermid syndrome, conditions associated with impairments in social memory. Shank3B knockout (KO) mice exhibit several behavioral abnormalities that may be analogous to symptoms of ASD, including social discrimination deficits. The CA2 region of the hippocampus integrates numerous afferents and sends a major output to the ventral CA1 (vCA1), circuitry that plays an important role in social memory. Despite finding few differences in excitatory afferents to the CA2 in Shank3B KO mice, chemogenetic activation of CA2 excitatory neurons restored social recognition function to wildtype (WT) levels. Specific activation of the CA2-vCA1 circuitry had a similar effect. Neuronal oscillations in the theta, gamma and, sharp wave ripple ranges have been linked to social memory, but we observed no differences in these measures between WT and Shank3B KO mice in the vCA1 in response to social stimuli. However, activation of CA2 excitatory neurons enhanced vCA1 theta power in Shank3B KO mice, concurrent with behavioral improvements. These findings suggest that stimulating adult circuitry in a mouse model with neurodevelopmental impairments can be sufficient to invoke latent function, particularly with respect to social memory dysfunction. The extent to which vCA1 network oscillations in the theta range are responsible for rescued behavioral function remains unknown.

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“…In addition, these individuals also show lower cortical thickness in the frontal regions, particularly the medial orbitofrontal region [31]. Others have not only reported functional and structural alterations in frontoparietal, fronto-limbic, fronto-striatal and cerebellar regions among adolescent cannabis users [32 & ], but also subcortical structures during rewardrelated processing [33]. Examining studies focusing on the emergence of substance, investigators found that altered neural structure and function of regions in reward processing, cognitive control and impulsivity can predate substance use initiation, escalation and disorder [34].…”

Section: Review or Meta-analysesmentioning

confidence: 99%

Neural substrates of substance use disorders

Paulus¹

2022

Current Opinion in Neurology

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Purpose of reviewSubstance use disorders account for a tremendous burden to society, yet despite substantial progress in basic studies, our understanding of the brain-basis of these disorders is still emerging. This review summarizes the recent findings of neuroimaging studies with substance use disorder individuals.Recent findingsResting-state functional connectivity studies support for some but not all substances of abuse and disruption in executive control. Structural neuroimaging findings point towards reduced subcortical volumes, which may emerge as an interaction between preexisting factors and recent substance use. Longitudinal studies implicate some of the same core brain structures and their functional role that have also been identified via case–control studies. Finally, meta-analyses support the idea of dysregulation of cortical control over subcortical salience processing.SummaryAlthough progress has been made and there is both structural and functional imaging evidence of an imbalance between brain structures involved in executive control and salience processing, there is emerging evidence that brain-behaviour relationships, which are core to discovering the neural processes that lead to and maintain substance use, are small and require larger consortia that prospectively examine individuals with substance use disorder.

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Atypical social reward anticipation as a transdiagnostic characteristic of psychopathology: A meta-analytic review and critical evaluation of current evidence

Cited by 89 publications

References 111 publications

Social thinning and stress generation after childhood maltreatment: a neurocognitive social transactional model of psychiatric vulnerability

Social thinning and stress generation after childhood maltreatment: a neurocognitive social transactional model of psychiatric vulnerability

Activation of the CA2-vCA1 pathway reverses social discrimination dysfunction inShank3Bknockout mice

Neural substrates of substance use disorders

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