Our study aimed to explore the recognition of specific emotions across the course of psychosis. A visual task representing the six basic emotions was used to assess facial emotion recognition (FER) in 204 healthy controls classified into 152 low-risk (LR) and 52 high-risk for psychosis (HR), following a psychometric risk approach; and 100 patients: 44 with first-episode psychosis (FEP) and 56 with multi-episode schizophrenia-spectrum disorders (MES). First, we performed a MANCOVA to compare the four conditions. Next, we conducted a logistic regression to explore whether specific FER deficits predicted the presence of psychosis. Finally, we investigated the relationships of FER with psychosis-like experiences (PLEs) and psychotic symptoms. Global FER, anger and fear recognition were impaired in HR, FEP and MES. No differences between HR and FEP appeared. Moreover, fear and anger correctly classified 83% of individuals into LR or psychosis. FER was associated with PLEs and psychotic symptoms. Concluding, FER is early impaired in HR individuals and increases along the psychosis continuum. However, fear recognition is similarly impaired throughout the illness, suggesting a possible vulnerability marker. Furthermore, deficits in anger and fear recognition predicted the presence of psychosis. Therefore, we suggest that FER may be essential in detecting psychosis risk.
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http://dx.doi.org/10.1016/j.psychres.2022.115029 | DOI Listing |
J Nutr
January 2025
Department of Physiology and Oral Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima 734-8553, Japan.
Background: Modern dietary trends have led to an increase in foods that are relatively high in n-6 polyunsaturated fatty acids (PUFAs) and low in n-3 PUFAs. We previously reported that the offspring of mother mice that consumed a diet high in n-6 linoleic acid (LA) and low in n-3 α-linolenic acid (ALA), hereinafter called the LA/ALA diet, exhibit behavioral abnormalities related to anxiety and feeding.
Objective: We currently lack a comprehensive overview of the behavioral abnormalities in these offspring, which was investigated in this study.
Behav Res Methods
January 2025
Department of Psychology, University of Quebec at Trois-Rivières, Trois-Rivières, Canada.
Frequently, we perceive emotional information through multiple channels (e.g., face, voice, posture).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Iowa, Iowa City, IA, USA.
Background: Sorbs2 is a cytoskeletal adaptor protein that is expressed in hippocampal neurons, but its mechanistic role in these cells is not yet fully understood.
Method: We created two groups of mice for our study: whole-body Sorbs2-Knockout (KO) mice and Sorbs2-Flox mice, which had neuronal knockout via AAV-PHP.eB-hSyn1-Cre virus injection.
Alzheimers Dement
December 2024
First Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang, China.
Background: Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), Smad4, a central intracellular signal transmission mediator of transmission of transforming growth factor-β (TGF-β) signaling, plays a pivotal role in many biological processes, including cell differentiation, migration, apoptosis and tumorigenesis. Emerging evidence has demonstrated that Smad4 is also involved in the pathogenesis of AD. Once TGF-β signaling is stimulated, Smad4 interaction with Sp1 and Smad3 induces the transcriptional activation of APP.
View Article and Find Full Text PDFBackground: Extracellular vesicles (EVs) carry pathogenic molecules and play a role in the disease spread, including aggregated tau proteins. The Endosomal Sorting Complexes Required for Transport (ESCRT) machinery is responsible for the biogenesis of small EVs (exosomes), thus targeting critical ESCRT molecules can disrupt EV synthesis. We hypothesize that microglia-specific targeting of ESCRT-I molecule Tsg101 suppresses microglia-derived EV-mediated propagation of tau pathology, leading to amelioration of the disease phenotype of the tauopathy mouse model.
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