The inhibition hypothesis advocated by Ekman (1985) states when an emotion is concealed or masked, the true emotion is manifested as a micro-expression (ME) which is a fleeting expression lasting for 40 to 500 ms. However, research about the inhibition hypothesis of ME from the perspective of electrophysiology is lacking. Here, we report the electrophysiological evidence obtained from an electroencephalography (EEG) data analysis method. Specifically, we designed an ME elicitation paradigm to collect data of MEs of positive emotions and EEG from 70 subjects, and proposed a method based on tensor component analysis (TCA) combined with the Physarum network (PN) algorithm to characterize the spatial, temporal, and spectral signatures of dynamic EEG data of MEs. The proposed TCA-PN methods revealed two pathways involving dorsal and ventral streams in functional brain networks of MEs, which reflected the inhibition processing and emotion arousal of MEs. The results provide evidence for the inhibition hypothesis from an electrophysiological standpoint, which allows us to better understand the neural mechanism of MEs.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.neulet.2022.136897 | DOI Listing |
Alzheimers Dement
December 2024
University of Manitoba, Winnipeg, MB, Canada.
Background: Mitochondrial bioenergetics are essential for cellular function, specifically the intricacies of the electron transport chain (ETC), with Complex IV playing a crucial role in unraveling the mechanisms governing energy production. Mathematical models offer a valuable approach to simulate these complex processes, providing insights into normal mitochondrial function and aberrations associated with various diseases, including neurodegenerative disorders. Our research focuses on introducing and refining a mathematical model, emphasizing Complex IV in the ETC, with objectives including incorporating mitochondrial activity modulation using inhibiting and uncoupling reagents, akin to oxygen consumption experiments.
View Article and Find Full Text PDFBackground: Recently, a highly significant brain proteome divergent modules change between Alzheimer's disease (AD) and CRND8 APP transgenic mice has been found. The M42 module is the module in human AD most highly correlated with amyloid and tau pathologies and cognitive decline. Among all proteins in this module, the (SPARC-related modular calcium-binding protein 1) SMOC1 is emerging as a robust biomarker of amyloid deposition in CSF.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Linkoping University, Linkoping, Sweden.
Background: Excessive dietary fat is not only a risk factor for metabolic disorders but also for premature cognitive decline and Alzheimer's disease. Recent findings from our study revealed that even a few days of a high-fat diet (HFD) are sufficient to disrupt hippocampal bioenergetics, activate microglia, and induce cognitive decline in mice. We hypothesize that microglia, rather than merely responding to diet-induced damage, play a critical role in disrupting synaptic homeostasis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Northwestern University, Chicago, IL, USA.
Background: Aging is the most significant risk factor for neurodegenerative tauopathies, including Alzheimer's disease (AD), frontotemporal dementia (FTD), progressive supranuclear palsy (PSP), and others. However, no specific age-related molecular change in the brain has been identified that leads to disease onset and progression. We have found age-related increases in bone morphogenic protein (BMP) signaling in both human and mouse brains.
View Article and Find Full Text PDFAtten Percept Psychophys
January 2025
Department of Psychology, Senshu University, Kawasaki, Japan.
Directional judgments of an arrow became slower when the direction and location were incongruent in a spatial Stroop task (i.e., a standard congruency effect).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!