This study provides a close look at the neural underpinning of the modulation of facial emotional mimicry by group membership and highlights the role of rTPJ in on-line control of co-activated self and other representations in social cognition.The present study has been designed to disentangle cognitive and emotional dimensions of empathy in a group of mentally healthy and highly alexithymic individuals (ALEX, n = 24) and well-matched controls (n = 26) through questionnaire Interpersonal Reactivity Index (IRI) and Multifaceted Empathy Task (MET) used during the fMRI and after the fMRI. Simultaneously, Skin Conductance Response (SCR) has been acquired as an implicit measure of emotional reaction. Results show an impaired emotional empathic ability in alexithymic individuals, with lower levels of SCR and higher activation in prefrontal brain regions such as the ventrolateral prefrontal cortex (VLPFC) and inferior frontal gyrus (IFG). Cognitive empathy was not impaired in the alexithymic group and the results were accompanied by a higher activation left IFG. The study leads to the conclusion that alexithymia does not only involve a diminished ability to identify and describe one’s own emotions. Furthermore, it is related to a deeper disability of emotion regulation, which becomes visible through impaired emotional concern for others and higher levels of personal distress.This study analyzes how people’s attitudes to the European refugee crisis (ERC) correspond to selected psychological state and trait measures and impact the neural processing of media images of refugees. From a large pool of respondents, who filled in an online xenophobia questionnaire, we selected two groups (total N = 38) with the same socio-demographic background, but with opposite attitudes toward refugees. We found that a negative attitude toward refugees (high xenophobia – HX) was associated with a significantly higher conscientiousness score and with a higher trait aggression and hostility, but there was no group effect connected with empathy, fear, and anxiety measures. At the neural level we found that brain activity during the presentation of ERC stimuli is affected by xenophobic attitudes-with more xenophobic subjects exhibiting a higher BOLD response in the left fusiform gyrus. However, while the fMRI results demonstrate increased attention and vigilance toward ERC-related stimuli in the HX group, they do not show differentiated patterns of brain activity associated with perception of dehumanized outgroup.Alcohol use disorder (AUD) has been associated with neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Prolonged excessive alcohol intake contributes to increased production of reactive oxygen species that triggers neuroimmune response and cellular apoptosis and necrosis via lipid peroxidation, mitochondrial, protein or DNA damage. Long term binge alcohol consumption also upregulates glutamate receptors, glucocorticoids and reduces reuptake of glutamate in the central nervous system, resulting in glutamate excitotoxicity, and eventually mitochondrial injury and cell death. In this review, we delineate the following principles in alcohol-induced neurodegeneration (1) alcohol-induced oxidative stress, (2) neuroimmune response toward increased oxidants and lipopolysaccharide, (3) glutamate excitotoxicity and cell injury, and (4) interplay between oxidative stress, neuroimmune response and excitotoxicity leading to neurodegeneration and (5) potential chronic alcohol intake-induced development of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease.Schizophrenia is a disorder with a heterogeneous etiology involving complex interplay between genetic and environmental risk factors. The immune system is now known to play vital roles in nervous system function and pathology through regulating neuronal and glial development, synaptic plasticity, and behavior. In this regard, the immune system is positioned as a common link between the seemingly diverse genetic and environmental risk factors for schizophrenia. Synthesizing information about how the immune-brain axis is affected by multiple factors and how these factors might interact in schizophrenia is necessary to better understand the pathogenesis of this disease. Such knowledge will aid in the development of more translatable animal models that may lead to effective therapeutic interventions. Selleck SGX-523 Here, we provide an overview of the genetic risk factors for schizophrenia that modulate immune function. We also explore environmental factors for schizophrenia including exposure to pollution, gut dysbiosis, maternal immune activation and early-life stress, and how the consequences of these risk factors are linked to microglial function and dysfunction. We also propose that morphological and signaling deficits of the blood-brain barrier, as observed in some individuals with schizophrenia, can act as a gateway between peripheral and central nervous system inflammation, thus affecting microglia in their essential functions. Finally, we describe the diverse roles that microglia play in response to neuroinflammation and their impact on brain development and homeostasis, as well as schizophrenia pathophysiology.Active memory forgetting is a well-regulated biological process thought to be adaptive and to allow proper cognitive functions. Recent efforts have elucidated several molecular players involved in the regulation of olfactory forgetting in Drosophila, including the small G protein Rac1, the dopamine receptor DAMB, and the scaffold protein Scribble. Similarly, we recently reported that dopaminergic neurons mediate both learning- and forgetting-induced plasticity in the mushroom body output neuron MBON-γ2α’1. Two open questions remain how does forgetting affect plasticity in other, highly plastic, mushroom body compartments and how do genes that regulate forgetting affect this cellular plasticity? Here, we show that forgetting reverses short-term synaptic depression induced by aversive conditioning in the highly plastic mushroom body output neuron MBON-γ1pedc>α/β. In addition, our results indicate that genetic tampering with normal forgetting by inhibition of small G protein Rac1 impairs restoration of depressed odor responses to learned odor by intrinsic forgetting through time passing and forgetting induced acutely by shock stimulation after conditioning or reversal learning.