Cognitive impairment is a core feature of schizophrenia that substantially accounts for poor functional outcomes associated with this disease in areas such as work, independent living and social relationships. Until recently, drug development in schizophrenia has focused on developing compounds that mainly target the positive psychotic symptoms of the illness. Although current antipsychotic drugs treat psychosis in schizophrenia rather well, their impact on cognitive dysfunction is minimal. In recent years there has been growing interest in developing novel treatments for cognitive deficits in schizophrenia. In this review we discuss pharmacologic strategies considered most likely to improve cognition. These putative molecular targets include receptors for acetylcholine, dopamine, glutamate, g-aminobutyric acid (GABA), serotonin and histamine. In addition, we propose that not only pharmacological, but also psychological treatments should be considered to enhance cognition in schizophrenia.
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http://dx.doi.org/10.2174/138920112800784772 | DOI Listing |
EClinicalMedicine
January 2025
College of Competitive Sports, Beijing Sport University, Beijing, China.
Background: Given the distinctive physiological characteristics of pregnant women, non-pharmacological therapies are increasingly being used to improve depressive and anxiety symptoms. Our objective was to explore and compare the impact of various non-pharmacological interventions in improving depressive and anxiety symptoms, and to identify the most effective strategies for pregnant women with depressive and/or anxiety symptoms.
Methods: We conducted a systematic search of PubMed, Embase, the Cochrane Library, and Web of Science for randomized controlled trials (RCTs) that compared non-pharmacological interventions to usual care, from the inception of each database up to October 5, 2024.
Genes Brain Behav
February 2025
Université Paris Cité, Institute of Psychiatry and Neuroscience of Paris (IPNP), Paris, France.
Schizophrenia is a frequent and disabling disease. The persistence of the disorder despite its harmful consequences represents an evolutionary paradox. Based on recent discoveries in genetics, scientists have formulated the "price-to-pay" hypothesis: schizophrenia would be intimately related to human evolution, particularly to brain development and human-specific higher cognitive functions.
View Article and Find Full Text PDFAnn Gen Psychiatry
January 2025
Department of Neuropsychiatry, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-Ku, Kumamoto, 860-8556, Japan.
Background: Seizure threshold increases with age and the frequency of electroconvulsive therapy (ECT). Therefore, therapeutic seizures can be difficult to induce, even at maximum stimulus charge with available ECT devices. Such cases are known as difficult-to-induce-seizures electroconvulsive therapy cases (DECs).
View Article and Find Full Text PDFPsych J
January 2025
Neuropsychology and Applied Cognitive Neuroscience Laboratory; CAS Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing, China.
Anhedonia is believed to be transdiagnostic symptom exist in various disorders including schizophrenia, major depressive disorder, and autism spectrum disorder. However, very few studies attempted to profile subclinical samples with schizophrenia, depressive, and autistic symptoms using measures of anhedonia scales. This study adopted a cluster analytical approach to examine the anhedonia profile in 46 individuals with schizotypal trait (ST), 43 subthreshold depression (SD), 27 autistic trait (AT), and 41 healthy controls.
View Article and Find Full Text PDFPsychoneuroendocrinology
January 2025
Department of Psychiatry, University Medical Center Groningen, Groningen, the Netherlands.
Background/objective: Raloxifene, a selective estrogen receptor modulator (SERM), may improve symptoms and cognition in schizophrenia spectrum disorders (SSD). Studies have shown inconsistent efficacy, especially in men with SSD. We assessed whether single nucleotide polymorphisms (SNPs) on genes involved in the pharmacodynamics (ESR1 and COMT) and pharmacokinetics (UGT1A8) of raloxifene can explain the heterogeneous treatment response to raloxifene augmentation in patients with SSD.
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