Reviews in the Neurosciences最新文献

Autism spectrum disorders (ASDs) are neurodevelopmental conditions characterized by deficits in social relationships and communication and restrictive, repetitive behaviors and interests. ASDs form a heterogeneous group from a clinical and genetic perspective. Currently, ASDs diagnosis is based on the clinical observation of the individual's behavior. The subjective nature of behavioral diagnoses, in the context of ASDs heterogeneity, contributes to significant variation in the age at ASD diagnosis. Early detection has been proved to be critical in ASDs, as early start of appropriate therapeutic interventions greatly improve the outcome for some children. Structural magnetic resonance imaging (MRI) is widely used in the diagnostic work-up of neurodevelopmental conditions, including ASDs, mostly for brain malformations detection. Recently, the focus of brain imaging shifted towards quantitative MRI parameters, aiming to identify subtle changes that may establish early detection biomarkers. ASDs have a strong genetic component; deletions and duplications of several genomic loci have been strongly associated with ASDs risk. Consequently, a multitude of neuroimaging and genetic findings emerged in ASDs in the recent years. The association of gross or subtle changes in brain morphometry and volumes with different genetic defects has the potential to bring new insights regarding normal development and pathomechanisms of various disorders affecting the brain. Still, the clinical implications of these discoveries and the impact of genetic abnormalities on brain structure and function are unclear. Here we review the literature on brain imaging correlated with the most prevalent genomic imbalances in ASD, and discuss the potential clinical impact.

Peripheral nerve injury, resulting from various physical and chemical causes, has a high incidence and significant functional impact. This injury, affecting both sensory and motor functions, can severely diminish quality of life and cause mental health issues. Consequently, it is a major focus of current research. Recent advancements in peripheral nerve repair technology, including the application of new techniques and materials, have expanded the options for nerve repair methods. A comprehensive article that combines the pathological process of peripheral nerve repair with these methods is needed to advance research in this field. This review aims to provide a comprehensive overview of various techniques for repairing peripheral nerve injuries. Beginning with the histopathology of nerve injury, it evaluates these techniques in detail to offer clinical guidance. This review summarizes the advantages and disadvantages of various peripheral nerve repair methods, including photobiological modulation therapy, suture repair, nerve graft repair, vein graft catheter repair, muscle graft repair, laser welding repair, nerve catheter repair, nerve sliding repair technology, growth factor-assisted repair, stem cell therapy, and exosome therapy. Additionally, it explores future directions in the treatment of peripheral nerve injuries, providing valuable references for experimental research and clinical treatment.

Intracranial atherosclerotic disease (ICAD) significantly increases the risk of ischemic stroke. It involves the accumulation of plaque within arterial walls and narrowing or blockage of blood vessel lumens. Accurate imaging is crucial for the diagnosis and management of ICAD at both acute and chronic stages. However, imaging the small, tortuous intracranial arterial walls amidst complex structures is challenging. Clinicians have employed diverse approaches to improve imaging quality, with a particular emphasis on optimizing the acquisition of images using new techniques, enhancing spatial and temporal resolution of images, and refining post-processing techniques. ICAD imaging has evolved from depicting lumen stenosis to assessing blood flow reserve and identifying plaque components. Advanced techniques such as fractional flow reserve (FFR), high-resolution vessel wall magnetic resonance (VW-MR), optical coherence tomography (OCT), and radial wall strain (RWS) now allow direct visualization of flow impairment, vulnerable plaques, and blood flow strain to plaque, aiding in the selection of high-risk stroke patients for intervention. This article reviews the progression of imaging modalities from lumen stenosis to vessel wall pathology and compares their diagnostic value for risk stratification in ICAD patients.

Glioblastoma is a brain cancer with a poor prognosis. Failure of classical chemotherapy and surgical treatments indicates that new therapeutic approaches are needed. Among cell-free options, exosomes are versatile extracellular vesicles (EVs) that carry important cargo across barriers such as the blood-brain barrier (BBB) to their target cells. This makes exosomes an interesting option for the treatment of glioblastoma. Moreover, exosomes can comprise many therapeutic cargos, including lipids, proteins, and nucleic acids, sampled from special intercellular compartments of their origin cell. Cells exposed to various immunomodulatory stimuli can generate exosomes enriched in specific therapeutic molecules. Notably, the secretion of exosomes could modify the immune response in innate and adaptive immune systems. For instance, glioblastoma-associated exosomes (GBex) uptake by macrophages could influence macrophage dynamics (e.g., shifting CD markers expression). Expression of critical immunoregulatory proteins such as cytotoxic T-lymphocyte antigen-1 (CTLA1) and programmed death-1 (PD-1) on GBex indicates the direct crosstalk of these nano-size vesicles with the immune system. The present study reviews the role of exosomes in immune system cells, including B cells, T cells, natural killer (NK) cells, and dendritic cells (DCs), as well as novel technologies in the field.

Variations in day length, or photoperiodism, whether natural or artificial light, significantly impact biological, physiological, and behavioral processes within the brain. Both natural and artificial light sources are environmental factors that significantly influence brain functions and mental well-being. Photoperiodism is a phenomenon, occurring either over a 24 h cycle or seasonally and denotes all biological responses of humans and animals to these fluctuations in day and night length. Conversely, artificial light occurrence refers to the presence of light during nighttime hours and/or its absence during the daytime (unnaturally long and short days, respectively). Light at night, which is a form of light pollution, is prevalent in many societies, especially common in certain emergency occupations. Moreover, individuals with certain mental disorders, such as depression, often exhibit a preference for darkness over daytime light. Nevertheless, disturbances in light patterns can have negative consequences, impacting brain performance through similar mechanisms albeit with varying degrees of severity. Furthermore, changes in day length lead to alterations in the activity of receptors, proteins, ion channels, and molecular signaling pathways, all of which can impact brain health. This review aims to summarize the mechanisms by which day length influences brain functions through neural circuits, hormonal systems, neurochemical processes, cellular activity, and even molecular signaling pathways.

The effectiveness of the support stimulation of the mechanoreceptors of the feet has been first shown in space medicine. In space flight during support withdrawal with non-use of postural muscle, this method is a countermeasure against sensorimotor disorders. Later, it was applied in clinical practice as treatment of motor disorders after stroke, in Parkinson's disease, infantile cerebral palsy, neuropathies, and many others. The impact of such stimulation on motor control is due to spinal and supraspinal mechanisms, which are activated by creating an additional support afferent input through the plantar surface. Many studies confirmed the positive effect of support stimulation on motor control, but the protocols of such stimulation remain the subject of active discussion. This review includes (1) the features of sensitivity of the foot sole cutaneous afferents to the support mechanical stimuli, (2) data on spinal and supraspinal responses of the nervous system to support stimulation, and (3) the results of applying this approach in neurological practice via various techniques. Summarizing this information, the authors highlight the most promising ways and types of medical devices for foot support stimulation in neurology.

In the ever-evolving landscape of deep learning (DL), the transformer model emerges as a formidable neural network architecture, gaining significant traction in neuroimaging-based classification and regression tasks. This paper presents an extensive examination of transformer's application in neuroimaging, surveying recent literature to elucidate its current status and research advancement. Commencing with an exposition on the fundamental principles and structures of the transformer model and its variants, this review navigates through the methodologies and experimental findings pertaining to their utilization in neuroimage classification and regression tasks. We highlight the transformer model's prowess in neuroimaging, showcasing its exceptional performance in classification endeavors while also showcasing its burgeoning potential in regression tasks. Concluding with an assessment of prevailing challenges and future trajectories, this paper proffers insights into prospective research directions. By elucidating the current landscape and envisaging future trends, this review enhances comprehension of transformer's role in neuroimaging tasks, furnishing valuable guidance for further inquiry.

The inhibitory avoidance (IA) task is a paradigm widely used to investigate the molecular and cellular mechanisms involved in the formation of long-term memory of aversive experiences. In this review, we discuss studies on different brain structures in rats associated with memory consolidation, such as the hippocampus, striatum, and amygdala, as well as some cortical areas, including the insular, cingulate, entorhinal, parietal and prefrontal cortex. These studies have shown that IA training triggers the release of neurotransmitters, hormones, growth factors, etc., that activate intracellular signaling pathways related to protein kinases, which induce intracellular non-genomic changes or transcriptional mechanisms in the nucleus, leading to the synthesis of proteins. We have summarized the temporal dynamics and crosstalk among protein kinase A, protein kinase C, mitogen activated protein kinase, extracellular-signal-regulated kinase, and Ca²⁺/calmodulin-dependent protein kinase II described in the hippocampus. Protein kinase activity has been associated with structural changes and synaptic strengthening, resulting in memory storage. However, little is known about the molecular mechanisms involved in intense IA training, which protects memory from typical amnestic treatments, such as protein synthesis inhibitors, and induces increased spinogenesis, suggesting an unexplored mechanism independent of the genomic pathway. This highly emotional experience causes an extinction-resistant memory, as has been observed in some pathological states such as post-traumatic stress disorder. We propose that the changes in spinogenesis observed after intense IA training could be generated by protein kinases via non-genomic pathways.

Major depressive disorder (MDD) is a prevalent psychiatric disorder that has damage to people's quality of life. Tryptophan is the precursor to serotonin, a critical neurotransmitter in mood modulation. In mammals, most free tryptophan is degraded by the kynurenine pathway (KP), resulting in a range of metabolites involved in inflammation, immune response, and neurotransmission. The imbalance between quinolinic acid (QA), a toxic metabolite, and kynurenic acid (KynA), a protective metabolite, is a relevant phenomenon involved in the pathophysiology of MDD. Proinflammatory cytokines increase the activity of the enzyme indoleamine 2,3-dioxygenase (IDO), leading to the degradation of tryptophan in the KP and an increase in the release of QA. IDO activates proinflammatory genes, potentiating neuroinflammation and deregulating other physiological mechanisms related to chronic stress and MDD. This review highlights the physiological mechanisms involved with stress and MDD, which are underlying an imbalance of the KP and discuss potential therapeutic targets.

Effective communication between different cell types is essential for brain health, and dysregulation of this process leads to neuropathologies. Brain glial cells, including microglia and astrocytes, orchestrate immune defense and neuroimmune responses under pathological conditions during which interglial communication is indispensable. Our appreciation of the complexity of these processes is rapidly increasing due to recent advances in molecular biology techniques, which have identified numerous phenotypic states of both microglia and astrocytes. This review focuses on microglia-to-astrocyte communication facilitated by secreted neuroimmune modulators. The combinations of interleukin (IL)-1α, tumor necrosis factor (TNF), plus complement component C1q as well as IL-1β plus TNF are already well-established microglia-derived stimuli that induce reactive phenotypes in astrocytes. However, given the large number of inflammatory mediators secreted by microglia and the rapidly increasing number of distinct functional states recognized in astrocytes, it can be hypothesized that many more intercellular signaling molecules exist. This review identifies the following group of cytokines and gliotransmitters that, while not established as interglial mediators yet, are known to be released by microglia and elicit functional responses in astrocytes: IL-10, IL-12, IL-18, transforming growth factor (TGF)-β, interferon (IFN)-γ, C-C motif chemokine ligand (CCL)5, adenosine triphosphate (ATP), l-glutamate, and prostaglandin E2 (PGE2). The review of molecular mechanisms engaged by these mediators reveals complex, partially overlapping signaling pathways implicated in numerous neuropathologies. Additionally, lack of human-specific studies is identified as a significant knowledge gap. Further research on microglia-to-astrocyte communication is warranted, as it could discover novel interglial signaling-targeted therapies for diverse neurological disorders.