Schizophrenia is a heartbreaking, debilitating, youth-stealing, lifetime disorder for most individuals afflicted with it. While the serendipitous discovery of chlorpromazine 60 plus years ago and the subsequent “discoveries” since have significantly reduced positive symptoms, the devastation of negative/cognitive symptoms continues to ruin lives. Given the cost in lives and dollars that schizophrenia drains out of our society, neuroscientists will continue to explore better approaches to fighting this disorder. The hypoglutamate model appears promising, yet there are miles to go before we sleep. As Nestler et al. (2009, p. 398) deftly acknowledge, “. . . it is important to point out that postulating a role for abnormal glutamatergic neurotransmission in schizophrenia is akin to proposing that the brain is involved in schizophrenia since every single neuron in the brain receives thousands of excitatory synapses that utilize glutamate as their neurotransmitter.”
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1744-6163.2012.00333.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Construction of a troublemaking risk assessment tool for patients with severe mental disorders in community of China.
Sci Rep
January 2025
Affiliated Mental Health Center of Jiangnan University, Wuxi Central Rehabilitation Hospital, Wuxi, 214151, Jiangsu, China.
Objective: Construction a troublemaking risk assessment tool to predict the risk of troublemaking for patients with severe mental disorders in the community of China.
Methods: 28,000 cases registered in the Jiangsu Provincial Severe Mental Disorder Management System from January 2017 to December 2019 were collected. The risk factors of troublemaking among patients with severe mental disorders in the community were analyzed through Logistic regression analysis, then the troublemaking risk assessment tool was established and verified.
Gene-level analysis reveals the genetic aetiology and therapeutic targets of schizophrenia.
Nat Hum Behav
January 2025
Department of Psychosomatics and Psychiatry, Zhongda Hospital, School of Medicine, Jiangsu Provincial Key Laboratory of Brain Science and Medicine, Advanced Institute for Life and Health, Southeast University, Nanjing, China.
Genome-wide association studies (GWASs) have reported multiple risk loci for schizophrenia (SCZ). However, the majority of the associations were from populations of European ancestry. Here we conducted a large-scale GWAS in Eastern Asian populations (29,519 cases and 44,392 controls) and identified ten Eastern Asian-specific risk loci, two of which have not been previously reported.
View Article and Find Full Text PDFInvestigating the causal pathways among psychopathological variables, cognitive impairment, and real-life functioning in people with schizophrenia.
Schizophrenia (Heidelb)
January 2025
Department of Psychiatry, University of Campania "Luigi Vanvitelli", 80138, Naples, Italy.
The present study aimed to investigate the causal relationships among cognitive impairment, psychopathology, and real-life functioning in a large sample of people with schizophrenia, using a data-driven causal discovery procedure based on partial ancestral graphs (PAGs). This method may provide additional insights for the identification of potential therapeutic targets to promote recovery in people with chronic schizophrenia. State-of-the-art instruments were used to assess the study variables.
View Article and Find Full Text PDFFXR1 Deletion from Cortical Parvalbumin Interneurons Modifies their Excitatory Synaptic Responses.
eNeuro
January 2025
Department of Neuroscience, University of Wisconsin-Madison, Madison, WI, 53705
Fragile X autosomal homolog 1 (FXR1), a member of the fragile X messenger riboprotein 1 family, has been linked to psychiatric disorders including autism and schizophrenia. Parvalbumin (PV) interneurons play critical roles in cortical processing, and have been implicated in FXR1-linked mental illnesses. Targeted deletion of FXR1 from PV interneurons in mice has been shown to alter cortical excitability and elicit schizophrenia-like behavior.
View Article and Find Full Text PDFNetwork pharmacology and molecular docking to explore mechanisms of clozapine-induced cardiac arrest.
J Psychiatry Neurosci
January 2025
From the Computational Biology Centre and the Laboratory of Psychiatric-Neuroimaging-Genetic and Comorbidity, Tianjin Anding Hospital, Tianjin Mental Health Centre of Tianjin Medical University, Nankai University Affiliated Tianjin Anding Hospital, Tianjin, China.
Background: Clozapine is superior to all other antipsychotics in treating schizophrenia in terms of its curative efficacy; however, this drug is prescribed only as a last resort in the treatment of schizophrenia, given its potential to induce cardiac arrest. The mechanism of clozapine-induced cardiac arrest remains unclear, so we aimed to elucidate the potential mechanisms of clozapine-induced cardiac arrest using network pharmacology and molecular docking.
Methods: We identified and analyzed the overlap between potential cardiac arrest-related target genes and clozapine target genes.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!