Neuronal underpinnings of cognitive impairment and - improvement in mood disorders

Miskowiak, Kamilla Woznica; Petersen, Cecilia S

doi:10.1017/s1092852918001062

Cited by 48 publications

(60 citation statements)

References 131 publications

(375 reference statements)

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“…In a recent systematic review of functional magnetic resonance imaging (fMRI) studies of cognitiveimpairment and -improvement across mood disorders, we identified some promising neurocircuitry-based targets for future cognition treatments. 19 Abnormal (hypo-and hyper-) activation of the dorsal prefrontal cortex (PFC) and failure to suppress the default mode network (DMN) were consistently observed across mood disorders and cognitive domains 19 (Figures 1 and 2). This finding is similar to that of a previous review article in depression by Fossati.…”

Section: Common Neural Correlates For Cognitive Impairments and Improvements Across Mood Disordersmentioning

confidence: 99%

Toward a transdiagnostic neurocircuitry-based biomarker model for pro-cognitive effects: challenges, opportunities, and next steps

Petersen

Miskowiak

2020

CNS Spectr.

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Cognitive impairment has emerged as a key treatment priority in neuropsychiatric disorders. However, there is a lack of treatments with solid and lasting efficacy on cognition. A neurocircuitry-based biomarker model of pro-cognitive effects is critically needed to select among new candidate treatments. In a recent review of functional magnetic resonance imaging (fMRI) studies in mood disorders, we found that cognitive impairments are consistently accompanied by aberrant (hypo- and hyper-) activity in the dorsal prefrontal cortex (PFC) and the default mode network (DMN), and that activity change in these regions commonly occurs with cognitive improvements. Here, we (i) review the putative model from our recent review article, which explains the discrepant findings regarding the direction of aberrant dorsal PFC activity and treatment-related activity change in mood disorders. Inspired by the Research Domain Criteria project, we do this in order to (ii) examine whether a similar pattern of activity change occurs across distinct neuropsychiatric disorders and thereby provides a common biomarker for pro-cognitive effects. Lastly, we (iii) discuss whether dorsal PFC and DMN target engagement is a putative transdiagnostic neurocircuitry-based biomarker model for pro-cognitive effects, and (iv) outline the necessary next steps to address this question.

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Section: Common Neural Correlates For Cognitive Impairments and Improvements Across Mood Disordersmentioning

confidence: 99%

Toward a transdiagnostic neurocircuitry-based biomarker model for pro-cognitive effects: challenges, opportunities, and next steps

Petersen

Miskowiak

2020

CNS Spectr.

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“…8 ), but systematic analyses of their incidence, life-progression and causal link with treatment are not yet available. It is likely that the aberrant function of cortico-thalamo-cortical networks (underlying the generation of SWD and absence seizures) ( Crunelli and Leresche, 2002 a ; Blumenfeld, 2005 a ) combines with the abnormal activity of basal ganglia-limbic-monoamine networks (underlying attention deficits, cognitive impairments and mood disorders) ( De Deurwaerdère et al , 2017 ; Miskowiak and Petersen, 2019 ; Park et al , 2019 ) to generate the overall neuropsychiatric comorbid phenotype of absence seizure ( Fig. 8 , left).…”

Section: Introductionmentioning

confidence: 99%

Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures

Crunelli

Lőrincz

McCafferty

et al. 2020

Brain

142

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Absence seizures in children and teenagers are generally considered relatively benign because of their non-convulsive nature and the large incidence of remittance in early adulthood. Recent studies, however, show that 30% of children with absence seizures are pharmaco-resistant and 60% are affected by severe neuropsychiatric comorbid conditions, including impairments in attention, cognition, memory and mood. In particular, attention deficits can be detected before the epilepsy diagnosis, may persist even when seizures are pharmacologically controlled and are aggravated by valproic acid monotherapy. New functional MRI-magnetoencephalography and functional MRI-EEG studies provide conclusive evidence that changes in blood oxygenation level-dependent signal amplitude and frequency in children with absence seizures can be detected in specific cortical networks at least 1 min before the start of a seizure, spike-wave discharges are not generalized at seizure onset and abnormal cortical network states remain during interictal periods. From a neurobiological perspective, recent electrical recordings and imaging of large neuronal ensembles with single-cell resolution in non-anaesthetized models show that, in contrast to the predominant opinion, cortical mechanisms, rather than an exclusively thalamic rhythmogenesis, are key in driving seizure ictogenesis and determining spike-wave frequency. Though synchronous ictal firing characterizes cortical and thalamic activity at the population level, individual cortico-thalamic and thalamocortical neurons are sparsely recruited to successive seizures and consecutive paroxysmal cycles within a seizure. New evidence strengthens previous findings on the essential role for basal ganglia networks in absence seizures, in particular the ictal increase in firing of substantia nigra GABAergic neurons. Thus, a key feature of thalamic ictogenesis is the powerful increase in the inhibition of thalamocortical neurons that originates at least from two sources, substantia nigra and thalamic reticular nucleus. This undoubtedly provides a major contribution to the ictal decrease in total firing and the ictal increase of T-type calcium channel-mediated burst firing of thalamocortical neurons, though the latter is not essential for seizure expression. Moreover, in some children and animal models with absence seizures, the ictal increase in thalamic inhibition is enhanced by the loss-of-function of the astrocytic GABA transporter GAT-1 that does not necessarily derive from a mutation in its gene. Together, these novel clinical and experimental findings bring about paradigm-shifting views of our understanding of absence seizures and demand careful choice of initial monotherapy and continuous neuropsychiatric evaluation of affected children. These issues are discussed here to focus future clinical and experimental research and help to identify novel therapeutic targets for treating both absence seizures and their comorbidities.

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“…Important information is maintained, while non-relevant stimuli must be suppressed or ignored. Dysfunctions of cognitive control (CC) processes are at the core of many psychopathological conditions [1,2], comprise the intentional selection of thoughts, emotions, and behaviours based on current task demands [3] involving functions of attention, memory, and emotional control [4], and are associated with altered patterns of brain activation [5,6]. The prefrontal cortex (PFC), particularly the dorsolateral prefrontal cortex (dlPFC), is known to be highly involved in CC processes [7] by means of processes related to working memory [8], encoding of task relevant rules and responses [9], and emotion regulation [10].…”

Section: Introductionmentioning

confidence: 99%

Enhancing cognitive control training with transcranial direct current stimulation: a systematic parameter study

2020

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Background: Cognitive control (CC) is an important prerequisite for goal-directed behaviour and efficient information processing. Impaired CC is associated with reduced prefrontal cortex activity and various mental disorders, but may be effectively tackled by transcranial direct current stimulation (tDCS)enhanced training. However, study data are inconsistent as efficacy depends on stimulation parameters whose implementations vary widely between studies. Objective: We systematically tested various tDCS parameter effects (anodal/cathodal polarity, 1/2 mA stimulation intensity, left/right prefrontal cortex hemisphere) on a six-session CC training combined with tDCS. Methods: Nine groups of healthy humans (male/female) received either anodal/cathodal tDCS of 1/2 mA over the left/right PFC or sham stimulation, simultaneously with a CC training (modified adaptive Paced Auditory Serial Addition Task [PASAT]). Subjects trained thrice per week (19 min each) for two weeks. We assessed performance progress in the PASAT before, during, and after training. Using a hierarchical approach, we incrementally narrowed down on optimal stimulation parameters supporting CC. Longterm CC effects as well as transfer effects in a flanker task were assessed after the training period as well as three months later. Results: Compared to sham stimulation, anodal but not cathodal tDCS improved performance gains. This was only valid for 1 mA stimulation intensity and particularly detected when applied to the left PFC. Conclusions: Our results confirm beneficial, non-linear effects of anodal tDCS on cognitive training in a large sample of healthy subjects. The data consolidate the basis for further development of functionally targeted tDCS, supporting cognitive control training in mental disorders and guiding further development of clinical interventions.

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Neuronal underpinnings of cognitive impairment and - improvement in mood disorders

Cited by 48 publications

References 131 publications

Toward a transdiagnostic neurocircuitry-based biomarker model for pro-cognitive effects: challenges, opportunities, and next steps

Toward a transdiagnostic neurocircuitry-based biomarker model for pro-cognitive effects: challenges, opportunities, and next steps

Clinical and experimental insight into pathophysiology, comorbidity and therapy of absence seizures

Enhancing cognitive control training with transcranial direct current stimulation: a systematic parameter study

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