Band 36, Heft 6

Auditory steady-state response (ASSR) is a robust method to probe gamma (>30 Hz) activity in a controlled manner. While typically the magnitude and the phase synchronization over stimulus repetitions of ASSR is assessed, other measures are being investigated. One of them is phase-amplitude coupling (PAC), which reflects the interactions between lower frequency phase and higher frequency amplitude. Considering that the number of studies assessing PAC during auditory steady-state stimulation has grown recently, in the present work, we aimed to perform a comprehensive overview of PAC methodological approaches in ASSR studies. We sought to evaluate the studies according to PAC analysis issues emphasized in empirical and theoretical PAC studies. Our work showed considerable variability in the methodology among the reviewed studies. Furthermore, the reviewed works address methodological issues and confounding factors of PAC relatively poorly and are characterized by insufficient descriptions of the applied approaches. Our review shows that systematic research of PAC in the context of ASSR is imperative in order to properly evaluate the presence of PAC during the auditory steady-state stimulation.

Within the concept of the extended mind, the active modification of external objects, externalizations, is seen as an auxiliary means to adapt to the environment. Toolmaking and use are advanced stages of externalizations that evolve. All past or present tools can, theoretically, be precisely assigned a location in an evolutionary tree with predecessors and progeny. Tools are reliably replicated, modified, and selected by their ability to facilitate human needs. Tool evolution, therefore, fulfills Darwinian criteria where the material tool is the phenotype and the instruction to build it is the code. The ostensive triangle consisting of a pointing individual, an observing individual, and a pointed-at object or tool is the germ cell of social transmission of instructions. Tool-building instructions ultimately can be reduced to distinct sequences of motor acts that can be recombined and are socially transmitted. When executed, they replicate tools for the reward of convenience or improved fitness. Tools elicit affordances relating to their use that synchronize different individuals’ perceptions, result in psychological “understanding,” and thereby modify social networks. Massive tool fabrication as present today in the “tool-sphere” has, therefore, accelerated prosociality and over time led to the acquisition of an individual’s third person perspective. The entangled biological evolution accelerated the ongoing cumulative cultural evolution by selecting traits facilitating social transmission. In this context, tool evolution and the corresponding acquired individual instructional content is a precondition to the emergence of higher cognition and “consciousness.” A neuroscience investigating externalizations as the starting point of this process is urgently needed.

This review explores the correlation of non-alcoholic fatty liver disease (NAFLD) with cognitive function and brain changes. A comprehensive search of relevant studies in the PubMed database up to June 2024 was conducted, including various study designs such as cross-sectional, longitudinal, case-control, and cohort studies. Data were extracted from 24 studies, focusing on study design, sample size, NAFLD diagnosis, control of confounders, key findings, and limitations. Neuropsychological tests utilized within each study were grouped into relevant cognitive domains. Statistical analyses and comparisons were also performed on the observed changes in brain parameters across the studies. The meta-analysis on the domain of general cognition was conducted. Results indicated that NAFLD was significantly associated with general cognition, executive function, attention, and memory. NAFLD impacts the total brain volume, the volumes of specific brain regions and certain high-intensity brain regions, the cerebral blood flow and perfusion, the integrity of nerve fiber bundles, and the brain abnormalities or lesions such as cerebral hemorrhage, cerebral microbleeds, and white matter lesions. NAFLD also affects the thickness and surface area of certain cortical regions and the resting-state brain function MRI indicators in specific brain areas. Despite these findings, the included studies varied in design, population characteristics, and outcome measures, which introduced heterogeneity that might influence the generalizability of the results. Overall, NAFLD is associated with a decline in cognitive function and alterations in certain brain parameters. Furthermore, NAFLD may exert its influence on cognition by impacting brain structure.

Epilepsy encompasses a group of chronic brain disorders characterized by recurrent, hypersynchronous activity of neuronal clusters, with epileptic seizures being the primary manifestation of these disorders. The objective of epilepsy treatment is to prevent seizures with minimum adverse side effects. However, approximately 30 % of patients do not respond to available medications. One proposed mechanism of epileptogenesis is glutamate excitotoxicity. When released in excess or not appropriately removed from the synaptic cleft, glutamate hyperactivates receptors, causing a biochemical cascade, which culminates in seizures and cell death. The use of animal models is essential for uncovering potential epileptogenic pathways, understanding the role of receptors and transporters in excitotoxicity, and screening effective antiepileptic treatments. This review examines studies that investigate the role of glutamate transporters and receptors in excitotoxicity and epileptogenesis using animal models. For this, we searched through both PubMed/Medline and ScienceDirect databases. After applying the inclusion and exclusion criteria, 26 (twenty-six) studies were selected for analysis. The studies addressed key glutamate transporter family of excitatory amino acid transporters (EAATs) EAAT1, EAAT2, and EAAT3, responsible for glutamate clearance, as well as AMPA receptor subunits GluA1 and GluA2, NMDA receptor subunits GluN1, GluN2a, and GluN2b, and the metabotropic receptors mGluR5 and mGluR2/3. Results showed that the dysregulation of these transporters and receptors is associated to seizure induction and excitotoxic damage, pointing to their fundamental role in the mechanisms of excitotoxicity and epileptogenesis. These findings highlight the potential of targeting glutamate transporters and receptors to stabilize glutamate homeostasis as an intervention in epilepsy management.

Dialectical thinking represents a cognitive style emphasizing change, contradiction, and holism. Cross-cultural studies reveal a stark contrast of dialectical thinking between East Asian and Western cultures, highlighting East Asians’ superior ability to embrace contradictions and foresee transformation, fostering psychological resilience through emotional complexity and tolerance for contradictions. Despite its importance, the neural basis of dialectical thinking remains underexplored. This review synthesizes current neuroscientific findings and introduces the dialectical-integration network (DIN) hypothesis, which identifies key brain regions such as the dorsal anterior cingulate cortex (dACC), medial prefrontal cortex (mPFC), dorsal lateral prefrontal cortex (DLPFC), nucleus accumbens, basal ganglia, and amygdala. These regions, along with networks like the default mode network (DMN) and frontoparietal network (FPN), facilitate holistic reasoning, conflict resolution, and sensory-emotional integration. The psychological benefits of dialectical thinking include enhanced cognitive flexibility, reduced emotional extremes, and improved conflict resolution. This review emphasizes the need for cross-cultural and neuroscientific research to explore the principle of change, a core aspect of dialectical cognition. By bridging cultural psychology and cognitive neuroscience, this work offers theoretical and methodological insights into culturally shaped cognitive styles, with practical applications in education, mental health, and intercultural communication. The DIN model provides a framework for future research on dynamic neural interactions supporting dialectical thinking.

Despite significant progress in managing HIV infection, HIV – associated neurocognitive disorder (HAND) continues to be a concern even among HIV individuals with well – controlled infection. Current diagnostic strategies, primarily reliant on neuropsychological tests, neuroimaging, and biomarkers from blood and cerebrospinal fluid, alongside combination antiretroviral therapy, form the foundation of HAND management. However, these strategies often fail to identify early or mild HAND, particularly asymptomatic neurocognitive impairment, resulting in delayed diagnosis and intervention. Furthermore, the inability to perform in-depth molecular analyses and conduct longitudinal tracking limits therapeutic advancements. Emerging technologies – advanced neuroimaging, multi-omics, artificial intelligence, alongside simian immunodeficiency virus non-human primate models – are revolutionizing the field. These innovations offer unprecedented opportunities for deeper understanding of the disease mechanism, early detection, comprehensive monitoring, and personalized treatment strategies. Integrating these cutting-edge tools promises to reshape the landscape of HAND management, enhancing the quality of life for those living with HIV.

Glutamate is not only the main excitatory neurotransmitter of the human central nervous system, but also a potent neurotoxin. Therefore, maintaining low-dose, non-toxic extracellular glutamate concentrations between synapses to ensure the reliability of synaptic transmission is essential for maintaining normal physiological functions of neurons. More and more studies have confirmed that the specific pathogenesis of central nervous system diseases (such as Alzheimer’s disease) caused by neuronal damage or death due to abnormal inter-synaptic glutamate concentration may be related to the abnormal function of excitatory amino acid transporter proteins and glutamine synthetase on astrocytes, and that the abnormal expression and function of the above two proteins may be related to the transcription, translation, and even modification of both by the process of transcription, translation, and even modification of astrocytes. oxidative stress, and inflammatory responses occurring in astrocytes during their transcription, translation and even modification. Therefore, in this review, we mainly discuss the relationship between glutamate metabolism (from postsynaptic neurons to astrocytes), Alzheimer’s disease and Parkinson’s disease in recent years.