RESUMO
Long-term aluminum (Al) exposure increases the risk of mild cognitive impairment (MCI). The aim of present study was to investigate the neural mechanisms of Al-induced MCI. In our study, a total of 52 individuals with occupational Al exposure > 10 years were enrolled and divided into two groups: MCI (Al-MCI) and healthy controls (Al-HC). Plasma Al concentrations and Montreal Cognitive Assessment (MoCA) score were collected for all participants. And diffusion tensor imaging and resting-state functional magnetic resonance imaging were used to examine changes of white matter (WM) and functional connectivity (FC). There was a negative correlation between MoCA score and plasma Al concentration. Compared with the Al-HC, fractional anisotropy value for the right fornix (cres)/stria terminalis (FX/ST) was higher in the Al-MCI. Furthermore, there was a difference in FC between participants with and without MCI under Al exposure. We defined the regions with differing FC as a "pathway", specifically the connectivity from the right temporal pole to the right FX/ST, then to the right sagittal stratum, and further to the right anterior cingulate and paracingulate gyri, and right inferior frontal gyrus, orbital part. In summary, we believe that the observed differences in WM integrity and FC in the right FX/ST between participants with and without MCI under long-term Al exposure may represent the neural mechanisms underlying MCI induced by aluminum exposure.Significance Statement Our study illuminates the neural "pathway" linking long-term aluminum exposure to mild cognitive impairment. Through integrated plasma aluminum assessments, cognitive evaluations, and advanced neuroimaging, we unveil differences in white matter integrity and functional connectivity, particularly in the right fornix/stria terminalis. These findings elucidate the neurobiological mechanisms underlying Al-induced MCI, highlighting the importance of addressing occupational Al exposure as a modifiable risk factor for cognitive decline.
Assuntos
Hérnia Inguinal , Herniorrafia , Hipertermia Maligna , Humanos , Hérnia Inguinal/cirurgia , Hérnia Inguinal/diagnóstico , Masculino , Herniorrafia/métodos , Herniorrafia/efeitos adversos , Hipertermia Maligna/etiologia , Hipertermia Maligna/diagnóstico , Pessoa de Meia-Idade , Parada Cardíaca/etiologia , Laparoscopia , VirilhaAssuntos
Pai , Gêmeos Monozigóticos , Humanos , Masculino , Marcadores Genéticos , Gêmeos Monozigóticos/genéticaRESUMO
Associative learning involves complex interactions of multiple cognitive factors. While adult subjects can articulate these factors verbally, for model animals such as macaques, we rely on behavioral outputs. In our study, we used pupillary responses as an alternative measure to capture these underlying cognitive changes. We recorded the dynamic changes in the pupils of three male macaques when they learned the associations between visual stimuli and reward sizes under the classical Pavlovian experimental paradigm. We found that during the long-term learning process, the gradual changes in the pupillary response reflect the changes in the cognitive state of the animals. The pupillary response can be explained by a linear combination of components corresponding to multiple cognitive factors. These components reflect the impact of visual stimuli on the pupils, the prediction of reward values associated with the visual stimuli, and the macaques' understanding of the current experimental reward rules. The changing patterns of these factors during interday and intraday learning clearly demonstrate the enhancement of current reward-stimulus association and the weakening of previous reward-stimulus association. Our study shows that the dynamic response of pupils can serve as an objective indicator to characterize the psychological changes of animals, understand their learning process, and provide important tools for exploring animal behavior during the learning process.
Assuntos
Aprendizagem por Associação , Cognição , Condicionamento Clássico , Pupila , Recompensa , Animais , Masculino , Aprendizagem por Associação/fisiologia , Pupila/fisiologia , Condicionamento Clássico/fisiologia , Cognição/fisiologia , Estimulação Luminosa/métodos , Macaca mulatta , Reflexo Pupilar/fisiologiaRESUMO
Hostile attribution bias refers to the tendency to interpret social situations as intentionally hostile. While previous research has focused on its developmental origins and behavioral consequences, the underlying neural mechanisms remain underexplored. Here, we employed functional near-infrared spectroscopy (fNIRS) to investigate the neural correlates of hostile attribution bias. While undergoing fNIRS, male and female participants listened to and provided attribution ratings for 21 hypothetical scenarios where a character's actions resulted in a negative outcome for the listener. Ratings of hostile intentions were averaged to measure hostile attribution bias. Using intersubject representational similarity analysis, we found that participants with similar levels of hostile attribution bias exhibited higher levels of neural synchrony during narrative listening, suggesting shared interpretations of the scenarios. This effect was localized to the left ventromedial prefrontal cortex (VMPFC) and was particularly prominent in scenarios where the character's intentions were highly ambiguous. We then grouped participants into high and low bias groups based on a median split of their hostile attribution bias scores. A similarity-based classifier trained on the neural data classified participants as having high or low bias with 75% accuracy, indicating that the neural time courses during narrative listening was systematically different between the two groups. Furthermore, hostile attribution bias correlated negatively with attributional complexity, a measure of one's tendency to consider multifaceted causes when explaining behavior. Our study sheds light on the neural mechanisms underlying hostile attribution bias and highlights the potential of using fNIRS to develop nonintrusive and cost-effective neural markers of this sociocognitive bias.