Neurocognition in schizophrenia: From prodrome to multi-episode illness

Corigliano, Valentina; Carolis, Antonella De; Trovini, Giada; Dehning, Julia; Pietro, Simone Di; Curto, Martina; Donato, Nicole; Pisa, Eleonora De; Girardi, Paolo; Comparelli, Anna

doi:10.1016/j.psychres.2014.07.067

Cited by 60 publications

(34 citation statements)

References 50 publications

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“…Cognitive decline begins in the prodromal stages with deficits in speed-of-processing, visuallearning and social-cognition in prodromal individuals (Corigliano et al 2014). In addition, cognitive functioning is highly associated with functional outcome in schizophrenia (Green et al 2004).…”

Section: Sex Differences In Symptom Domains and Severitymentioning

confidence: 99%

Sex differences in animal models of schizophrenia shed light on the underlying pathophysiology

Hill

2016

Neuroscience & Biobehavioral Reviews

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Section: Sex Differences In Symptom Domains and Severitymentioning

confidence: 99%

Sex differences in animal models of schizophrenia shed light on the underlying pathophysiology

Hill

2016

Neuroscience & Biobehavioral Reviews

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“…We compared overall cognitive function (primary outcome) as well as eight specific cognitive domains (secondary outcomes), between active drugs and placebo that were added to antipsychotics. Modifying the Measurement and Treatment Research to Improve Cognition in Schizophrenia domains, 37 we classified cognitive function into eight cognitive domains: (1) attention/vigilance, (2) cognitive control/executive function, (3) reasoning/problem solving, (4) social cognition, (5) speed of processing, (6) verbal learning, (7) visual learning, and (8) Table S1). If cognitive tests could not be assigned to any domain, they were excluded.…”

Section: Outcome Measuresmentioning

confidence: 99%

“…Cognitive impairment represents a core feature of schizophrenia, 1 is evident before the first episode of psychosis (FEP), 2 and has been reported to be one of the strongest predictors of functional outcome in schizophrenia. 3,4 The primary treatment for schizophrenia is antagonism of dopamine receptors with antipsychotic medications.…”

Section: Introductionmentioning

confidence: 99%

Effects of glutamate positive modulators on cognitive deficits in schizophrenia: a systematic review and meta-analysis of double-blind randomized controlled trials

et al. 2015

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Hypofunction of N-methyl-D-aspartate (NMDA) receptors has been proposed to have an important role in the cognitive impairments observed in schizophrenia. Although glutamate modulators may be effective in reversing such difficult-to-treat conditions, the results of individual studies thus far have been inconsistent. We conducted a systematic review and meta-analysis to examine whether glutamate positive modulators have beneficial effects on cognitive functions in patients with schizophrenia. A literature search was conducted to identify double-blind randomized placebo-controlled trials in schizophrenia or related disorders, using Embase, Medline, and PsycINFO (last search: February 2015). The effects of glutamate positive modulators on cognitive deficits were evaluated for overall cognitive function and eight cognitive domains by calculating standardized mean differences (SMDs) between active drugs and placebo added to antipsychotics. Seventeen studies (N = 1391) were included. Glutamate positive modulators were not superior to placebo in terms of overall cognitive function (SMD = 0.08, 95% confidence interval = − 0.06 to 0.23) (11 studies, n = 858) nor each of eight cognitive domains (SMDs = − 0.03 to 0.11) (n = 367-940) in this population. Subgroup analyses by diagnosis (schizophrenia only studies), concomitant antipsychotics, or pathway of drugs to enhance the glutamatergic neurotransmission (glycine allosteric site of NMDA receptors or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors) suggested no procognitive effect of glutamate positive modulators. Further, no effect was found in individual compounds on cognition. In conclusion, glutamate positive modulators may not be effective in reversing overall cognitive impairments in patients with schizophrenia as adjunctive therapies.

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“…Neurocognitive deficits are a key clinical feature of schizophrenia that predate the onset of psychosis and predict long-term disability in patients (Corigliano et al, 2014; Eastvold et al, 2007; Green, 1996; Green et al, 2004; Jahshan et al, 2010; Nuechterlein et al, 2014). Existing antipsychotics and nootropics however have limited efficacy in improving cognition and functional outcomes in schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Impaired hippocampal-dependent memory and reduced parvalbumin-positive interneurons in a ketamine mouse model of schizophrenia

Koh

Shao

Sherwood

et al. 2016

Schizophrenia Research

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The hippocampus of patients with schizophrenia displays aberrant excess neuronal activity which affects cognitive function. Animal models of the illness have recapitulated the overactivity in the hippocampus, with a corresponding regionally localized reduction of inhibitory interneurons, consistent with that observed in patients. To better understand whether cognitive function is similarly affected in these models of hippocampal overactivity, we tested a ketamine mouse model of schizophrenia for cognitive performance in hippocampal- and medial prefrontal cortex (mPFC)-dependent tasks. We found that adult mice exposed to ketamine during adolescence were impaired on a trace fear conditioning protocol that relies on the integrity of the hippocampus. Conversely, the performance of the mice was normal on a delayed response task that is sensitive to mPFC damage. We confirmed that ketamine-exposed mice had reduced parvalbumin-positive interneurons in the hippocampus, specifically in the CA1, but not in the mPFC in keeping with the behavioral findings. These results strengthened the utility of the ketamine model for preclinical investigations of hippocampal overactivity in schizophrenia.

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Neurocognition in schizophrenia: From prodrome to multi-episode illness

Cited by 60 publications

References 50 publications

Sex differences in animal models of schizophrenia shed light on the underlying pathophysiology

Sex differences in animal models of schizophrenia shed light on the underlying pathophysiology

Effects of glutamate positive modulators on cognitive deficits in schizophrenia: a systematic review and meta-analysis of double-blind randomized controlled trials

Impaired hippocampal-dependent memory and reduced parvalbumin-positive interneurons in a ketamine mouse model of schizophrenia

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