Neuroscience
-
The Weak Central Coherence account of autism spectrum disorders posits that individuals with ASD utilize a detail-oriented information processing bias. While this local bias is helpful in visual search tasks, ASD individuals falter in social cognition tasks where coherence is advantageous. The present study examined the neural correlates of Weak Central Coherence in ASD during visual and social processing. ⋯ The TD group showed significantly increased areas of activity over the ASD group in the Shape task in regions associated with executive control, such as the medial prefrontal cortex and middle frontal gyrus, suggesting increased interference from the global/social information. During the Emotion condition, the ASD group showed decreased connectivity between frontal and posterior regions and between body perception and motor networks, suggesting a possible difference in mirroring. The findings suggest that social cognitive factors, not visual processing biases, underlie the observed behavioral differences.
-
Individuals show marked variability in determining to be honest or deceptive in daily life. A large number of studies have investigated the neural substrates of deception; however, the brain networks contributing to the individual differences in deception remain unclear. In this study, we sought to address this issue by employing a machine-learning approach to predict individuals' deceptive propensity based on the topological properties of whole-brain resting-state functional connectivity (RSFC). ⋯ The machine-learning model sufficiently decoded individual differences in deception using three brain networks based on RSFC, including the executive controlling network (dorsolateral prefrontal cortex, middle frontal cortex, and orbitofrontal cortex), the social and mentalizing network (the temporal lobe, temporo-parietal junction, and inferior parietal lobule), and the reward network (putamen and thalamus). These networks have been found to form a signaling cognitive framework of deception by coding the mental states of others and the reward or values of deception or honesty, and integrating this information to make a final decision about being deceptive or honest. These findings suggest the potential of using RSFC as a task-independent neural trait for predicting deceptive propensity, and shed light on using machine-learning approaches in deception detection.
-
Alzheimer's disease is a chronic neurological ailment that seriously threatens human health and imposes a huge burden on families and the society at large. Emerging evidence suggests that neuroinflammation is an important pathological manifestation of neurodegenerative diseases, and currently considered a new research target. We previously found that artemisinin B from Artemisia annua Linn. has strong anti-inflammatory and immunological activities. ⋯ This study also showed that artemisinin B improved spatial memory in dementia mice in the water maze and step-through tests, and altered the pathological features and the levels of inflammatory cytokines in the hippocampus and the cortex. These results suggested that artemisinin B might inhibit neuroinflammation and exert neuroprotective effects on cognitive functions by modulating the TLR4-MyD88-NF-κB signaling pathway. This study provides direct evidence for the potential application of artemisinin B in the treatment of neuroinflammatory diseases.
-
Primary cultures of rat dorsal root ganglia (DRG) consist of neurons, satellite glial cells and a moderate number of macrophages. Measurements of increased intracellular calcium [Ca2+]i induced by stimuli, have revealed that about 70% of DRG neurons are capsaicin-responsive nociceptors, while 10% responded to cooling and or menthol (putative cold sensors). Cultivation of DRG in the presence of a moderate dose of lipopolysaccharide (LPS, 1 µg/ml) enhanced capsaicin-induced Ca2+ signals. ⋯ In the presence of the cytotoxic agent cisplatin (5 or 10 µg/ml), the number of macrophages was decreased significantly, the growth of satellite glial cells was markedly suppressed, but the vitality and stimulus-induced Ca2+ signals of DRG neurons were not impaired. Under these conditions the LPS-induced production and expression of TNF-α and IL-6 were blunted. Our data suggest a potential role for macrophages and satellite glial cells in the initiation of inflammatory processes that develop in sensory ganglia upon injury or exposure to pathogens.