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Based on the mind-blindness hypothesis, a large number of studies have shown that individuals with autism-spectrum disorder (ASD) and autistic traits have empathy deficits. However, the recent double empathy theory contradicts the mind-blindness hypothesis and suggests that individuals with ASD and autistic traits do not necessarily lack empathy. Thus, the presence of empathy deficits in individuals with ASD and autistic traits is still controversial. We recruited 56 adolescents (28 high autistic traits, 28 low autistic traits, 14-17 years old) in this study to explore the relationship between empathy and autistic traits. The study participants were required to undertake the pain empathy task, during which the electroencephalograph (EEG) activities were recorded. Our results show that empathy was negatively associated with autistic traits at the questionnaire, behavioral, and EEG levels. Our results also suggested that empathy deficits in adolescents with autistic traits may be manifested mainly in the late stages of cognitive control processing., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Experimental modeling and clinical neuroimaging of patients has shown that certain seizures are capable of causing neuronal death. Research into cell death after seizures has identified the induction of the molecular machinery of apoptosis. Temporal lobe epilepsy (TLE) is the most common type of epilepsy in adults, which is characterized by substantial pathological abnormalities in the temporal lobe, including the hippocampus and entorhinal cortex (EC). Although decades of studies have revealed numerous molecular abnormalities in the hippocampus that are linked to TLE, the biochemical mechanisms associated with TLE in EC remain unclear. In this study, we explored these early phenotypical alterations in the EC 5 days after mice were given a systemic injection of kainic acid (KA) to induce status epilepticus (KA-SE). we used the Tandem Mass Tag (TMT) combined with LC-MS/MS approach to identify distinct proteins in the EC in a mouse model of KA-SE model. According to the findings, 355 differentially abundant proteins including 199 upregulated and 156 downregulated differentially abundant proteins were discovered. The first-ranked biological process according to Gene Ontology (GO) analysis was "negative control of extrinsic apoptotic signaling". "Apoptosis" was the most significantly enriched Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway. Compared with those in control mice, BCL2L1, NTRK2 and MAPK10 abundance levels were reduced in KA mice. MAPK10 and NTRK2 act as upstream regulators to regulate BCL2L1, and BCL2L1 Inhibits cell death by blocking the voltage- dependent anion channel (VDAC) and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. However, ITPR1 was increased at the mRNA and protein levels in KA mice. Furthermore, there was no significant difference in ACTB, TUBA1A and TUBA4A levels between the two groups. Our results offer clues to help identify biomarkers for the development of pharmacological therapies targeted at epilepsy., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Autosomal dominant lateral temporal epilepsy (ADLTE) is an inherited syndrome caused by mutations in the leucine-rich glioma inactivated 1 (LGI1) gene. In a family with six ADLTE patients spanning four generations, our linkage and exome sequencing investigations revealed a rare frameshift heterozygous mutation in LGI1 (c.1494del(p.Phe498LeufsTer15)). Gene cloning methods were used to create plasmids with wild-type and mutant LGI1 alleles. Through transfection of HEK293 cells and primary neurons, they were utilized to assess the subcellular location of wild-type and mutant LGI1. Moreover, the plasmid-transfected primary neurons were analyzed for neuronal complexity and density of dendritic spines. According to our results. the mutation decreased LGI1 secretion in transfected HEK293 cells. In primary neurons, mutant LGI1 affected neuronal polarity and complexity. Our findings have broadened the phenotypic spectrum of LGI1 mutations and provided evidence regarding the pathogenicity of this mutation. In addition, we discovered new information about the role of LGI1 in the development of temporal lobe epilepsy, along with a possible link between neuronal polarity disorder and ADLTE., (Copyright © 2022. Published by Elsevier B.V.)

Converging evidence from imaging, microarray, genetic, and other studies suggests that abnormalities in myelin may play a role in schizophrenia. The expression of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP), which is used as a myelin marker, has been reported to be reduced in the schizophrenic brain. A synonymous genetic variation in the CNP gene, rs2070106, has recently been shown to be associated with schizophrenia in Caucasians. The present study investigates whether this finding can be replicated in the Han Chinese population. We performed an association analysis of four ht-SNPs in the CNP gene in a Chinese sample consisting of 426 schizophrenic patients and 439 healthy controls. We did not find any significant differences in any genotypic, allelic or haplotypic distributions between patients and controls. Therefore, this study did not find an association between genetic variations in the CNP gene and schizophrenia in the Han Chinese population.

The present study examined the correlation between variants in the d-amino acid oxidase activator (DAOA) locus and clinical symptoms and response to antipsychotics in schizophrenia. Case-control analysis and the family-based association test (FBAT) were performed to investigate whether four single nucleotide polymorphisms (SNPs) at DAOA gene are associated with schizophrenia. The association between the DAOA risk haplotype and clinical symptoms were examined by the positive and negative syndrome scale (PANSS) and the brief psychiatric rating scale (BPRS). Our findings showed that the SNP rs947267 was significantly associated with schizophrenia in both case control and familial trio samples (A>C, chi(2)=8.36, p=0.004; Z=2.335, p=0.019), as well as with specific haplotypes, in particular those formed by the A allele of rs947267. In addition, the risk haplotype AAG was significantly correlated with negative, depression and cognitive impairment factors of PANSS, even with the BPRS change scores after 6-week treatment of atypical antipsychotic drugs (p<0.05). These results support the hypothesis that variations in DAOA may play a role in schizophrenia and clinical characteristics.

Streptozotocin-induced diabetes for 4 weeks resulted in a decrease in proopiomelanocortin (POMC) mRNA in both the anterior lobe (AL) and the neuro-intermediate lobe (NIL) of the rat pituitary. The beta-endorphin levels decreased in the NIL but not in the AL. It is concluded that the synthesis of POMC in the pituitary is inhibited in diabetic rats and that there is a decrease in beta-endorphin release from the anterior pituitary.

Immunohistochemical study of the distribution of glutamate receptor subunits 1-4 (GluR1-4), NMDA receptor subunit 1 and metabotropic glutamate receptor subtypes 1-3 (mGluR1-3) in the ependymal cells of the caudal medulla oblongata and upper thoracic spinal cord was carried out. The results showed that ependymal cells and tanycytes expressed only the metabotropic receptor subtype, mGluR1 alpha. Some of the mGluR1 alpha-positive long basal processes of the tanycytes reached the pia mater; some made contact with capillaries. It was suggested that the activity of the these mGluR 1 a-positive tanycytes may be regulated by the CSF and blood. The presence of many mGluR1 alpha positive fibres in the area postrema suggests that mGluR1 alpha subtype in this region may be involved in cardiovascular regulation.