Reviews in the Neurosciences最新文献

Tryptophan (TRP) metabolism produces various neuroactive substances in the gastrointestinal tract, as well as in the central and peripheral nervous systems and intestinal microbiota. Initially centered on the serotonin pathway in TRP metabolism and TRP itself, many studies are now focusing on the kynurenine pathway, with an increasing interest in the indole pathway. Several TRP metabolites have been associated with migraines, suggesting that TRP metabolism may serve as a potential therapeutic target. However, these studies have significant limitations, including a small number of participants, a lack of standardized diets prior to and/or during clinical trials, and insufficient information regarding the transformation of TRP after its intake. Furthermore, no thorough study encompasses all the essential components of TRP metabolism: products, enzymes, receptors, and transporters. Different mechanisms may explain the involvement of TRP metabolism in migraines, including glutamate signaling and neurovasodilatory, immune, oxidative, and inflammatory processes. The results of studies on the role of TRP metabolism in migraine may be helpful for making dietary recommendations for migraine prevention and clinical management; however, individual characteristics for metabolizing TRP should be considered. The aim of this narrative perspective review is to critically present the results of studies on the role of TRP metabolism in migraine and explore their implications for migraine prevention and therapy. Unlike many other reviews that focus solely on either the serotonin or kynurenine pathway, our paper addresses all three primary TRP metabolism pathways.

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.

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.

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.

Major depressive disorder is a common mental disorder, and a significant number of patients exhibit poor response to conventional antidepressant treatments, known as treatment-resistant depression (TRD). However, the definition of TRD globally remains unclear, impeding clinical research, treatment development, outcome implementation, and policy-making. A wealth of research confirms that rTMS demonstrates promising efficacy in TRD. This paper elucidates the definition of TRD, summarizes potential targets of rTMS for treating TRD, comprehensively elaborates on the unique mechanisms, efficacy, and side effects of rTMS in treating TRD, and outlines considerations for special populations receiving rTMS treatment for TRD as well as other treatment modalities for TRD. Through these studies, we aim to provide more scientifically grounded recommendations for patients undergoing rTMS treatment for TRD.

There has been a significant amount of attention directed towards understanding brain development, shedding light on the underlying mechanisms. The proliferation and differentiation of brain stem cells have been a key focus. The process of neurolation occurs during the early stages of embryonic development, leading to the formation of the neural tube, a hollow nerve cord that gives rise to the central nervous system (CNS). There is a growing emphasis on the fluid-filled space inside the developing CNS and the potential role of cerebrospinal fluid (CSF) in brain development. The flow of CSF near the germinal epithelium significantly impacts the proliferation of cells in the cerebral cortex. CSF provides crucial support to the germinal epithelium, influencing the growth and differentiation of neural stem cells. It achieves this by releasing growth factors, cytokines, and morphogens that control the proliferation, survival, and migration of neuroepithelium. During development, the concentration of proteins in the CSF is notably higher compared to that in adults. Studies have indicated that removing CSF from the brain's ventricles during development causes an increase in neural cell deaths and a reduction in neural cell proliferation, ultimately leading to a thinner cerebral cortex. Additionally, many researches demonstrate that the composition of the CSF is essential for maintaining germinal matrix function and output, highlighting the critical role of CSF in brain development. It is concluded that CSF impacts the proliferation and differentiation of neural stem cells, which in turn plays a pivotal role in brain development.

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.

Fast spiking parvalbumin (PV) interneuron is an inhibitory gamma-aminobutyric acid (GABA)ergic interneuron diffused in different brain networks, including the cortex and hippocampus. As a key component of brain networks, PV interneurons collaborate in fundamental brain functions such as learning and memory by regulating excitation and inhibition (E/I) balance and generating gamma oscillations. The unique characteristics of PV interneurons, like their high metabolic demands and long branching axons, make them too vulnerable to stressors. Neuroinflammation is one of the most significant stressors that have an adverse, long-lasting impact on PV interneurons. Neuroinflammation affects PV interneurons through specialized inflammatory pathways triggered by cytokines such as tumor necrosis factor (TNF) and interleukin 6 (IL-6). The crucial cells in neuroinflammation, microglia, also play a significant role. The destructive effect of inflammation on PV interneurons can have comprehensive effects and cause neurological disorders such as schizophrenia, Alzheimer's disease (AD), autism spectrum disorder (ASD), and bipolar disorder. In this article, we provide a comprehensive review of mechanisms in which neuroinflammation leads to PV interneuron hypofunction in these diseases. The integrated knowledge about the role of PV interneurons in cognitive networks of the brain and mechanisms involved in PV interneuron impairment in the pathology of these diseases can help us with better therapeutic interventions.