During the course of a larger study on sensory thresholds and transliminality, 22 men and 28 women (M = 23.1 yr., SD = 2.9) mostly composed of students selected from a snowball sampling approach completed the Revised Transliminality Scale and a brief measure of everyday aberrations in memory. Scores on the measures correlated .59 (p < .001), and this result was not due to the confounding effects of age or sex. These preliminary results are consistent with the hypothesis that transliminality involves a state of increased activation that can induce a loss of conscious experience, thereby lending support to the definition of transliminality as the tendency for psychological material to cross thresholds into or out of consciousness.
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http://dx.doi.org/10.2466/pms.2003.96.3c.1300 | DOI Listing |
LAIR1 is an inhibitory receptor broadly expressed on human immune cells, including B cells. LAIR1 has been shown to modulate BCR signaling, however, it is still unclear whether its suppressive activity can be a negative regulator for autoreactivity. In this study, we demonstrate the LAIR1 expression profile on human B cells and prove its regulatory function and relationships to B cell autoreactivity.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico.
The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
February 2025
Department of Histology and Embryology, Faculty of Basic Medical Sciences, Hubei University of Medicine, Shiyan, People's Republic of China.
The coexistence of Alzheimer's disease (AD) and chronic pain (CP) in the elderly population has been extensively documented, and a growing body of evidence supports the potential interconnections between these two conditions. This comprehensive review explores the mechanisms by which CP may contribute to the development and progression of AD, with a particular focus on neuroinflammatory pathways and the role of microglia, as well as the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome. The review proposes that prolonged pain processing in critical brain regions can dysregulate the activity of the NLRP3 inflammasome within microglia, leading to the overproduction of pro-inflammatory cytokines and excessive oxidative stress in these regions.
View Article and Find Full Text PDFJ Exp Psychol Gen
January 2025
Department of Cognitive Psychology, Institute of Psychology, Universitat Hamburg.
While prediction errors (PEs) have long been recognized as critical in associative learning, emerging evidence indicates their significant role in episodic memory formation. This series of four experiments sought to elucidate the cognitive mechanisms underlying the enhancing effects of PEs related to aversive events on memory for surrounding neutral events. Specifically, we aimed to determine whether these PE effects are specific to predictive stimuli preceding the PE or if PEs create a transient window of enhanced, unselective memory formation.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Neurobiology, Care Sciences and Society, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Alzheimer's disease (AD) is a neurodegenerative disorder clinically characterized by progressive decline of memory and cognitive functions, and it is the leading cause of dementia accounting for 60%-80% of dementia patients. A pathological hallmark of AD is the accumulation of aberrant protein/peptide aggregates such as extracellular amyloid plaques containing amyloid-beta peptides and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. These aggregates result from the failure of the proteostasis network, which encompasses protein synthesis, folding, and degradation processes.
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