Neuroscience最新文献

L-proline is an amino acid with a unique cyclic structure, involvement in various physiological processes, such as protein synthesis, collagen production, and neurotransmission. This review explores the complex roles of proline in the central nervous system (CNS), where it contributes to both excitatory and inhibitory neurotransmission. Additionally, L-proline has distinct metabolic functions attributed to its structural properties. The concentration-dependent effects of L-proline indicate its importance in CNS function, with potential implications for health and disease. Studies in animal models suggest that L-proline influences cognitive function and behavior, with dysregulated levels linked to learning and memory deficits. Furthermore, this review addresses the neuropathological consequences of hyperprolinemia, a metabolic disorder marked by elevated L-proline levels in the CNS and examines the potential role of L-proline in neurological and psychiatric disorders. In sum, this work provides a comprehensive perspective on the neurobiological importance of L-proline, underscoring its involvement in neurotransmission, behavioral modulation, and disease pathology.

Epilepsy is a primary study focus for scientists worldwide due to its prevalence and poor prognosis. Silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent deacetylase, is becoming increasingly recognized for its critical role in the pathophysiology and progression of epilepsy. The treatment of epilepsy remains challenging despite the discovery of numerous factors that contribute to the development of several beneficial medications. In recent years, many microRNAs have been linked to the progression of epilepsy because they target SIRT1 mRNA. SIRT1, which protects from epilepsy, has been reported to be upregulated by several natural compounds and their derivatives. This review will summarize the latest findings about SIRT1's role in epilepsy. Results from the literature indicate that SIRT1 is a promising target for epilepsy therapy.

Type 2 diabetes (T2D) is often accompanied by non-alcoholic fatty liver disease (NAFLD), both of which are related to brain damage and cognitive impairment. However, cortical structural alteration and its relationship with metabolism and cognition in T2D with NAFLD (T2NAFLD) and without NAFLD (T2noNAFLD) remain unclear. The brain MRI scans, clinical measures and neuropsychological test were evaluated in 50 normal controls (NC), 73 T2noNAFLD, and 58 T2NAFLD. The cortical thickness and graph theory properties of structural covariance network was calculated. Statistical analyses included one-way analysis of covariance with post hoc, partial correlation and mediation analysis. The nonparametric permutation test was performed to evaluate differences in topological properties of structural covariance network. We found T2NAFLD group had worse glucose and lipid profiles, more obesity and more severe insulin resistance, and poorer working memory compared to T2noNAFLD and NC. T2D patients demonstrated increase in cortical thickness compared to NC, but no difference between the two T2D groups. The structural covariance network integration decreased in T2D patients, with T2NAFLD exhibiting more obvious network reconfiguration at node level. Cortical thickness mediated the relationship between post-prandial glucose, waist-hip ratio, and working memory. The findings suggest that cortical thickening may be a compensatory response to reduced network integration, with NAFLD exacerbating regional structural network changes in T2D. This research advances our understanding of how these metabolic comorbidities contribute to cognitive decline, potentially guiding future therapeutic strategies for T2D patients with and without NAFLD.

Physical and motor fatigue are debilitating symptoms common in multiple sclerosis (MS). Lifestyle interventions may be effective in managing MS-related fatigue. This scoping review aims to: (i) identify and summarise lifestyle interventions including those focused on diet, physical activity, and sleep, or multicomponent interventions for physical and motor fatigue management in MS; and (ii) provide recommendations for future research in this area. Database searches of MEDLINE (Ovid), Cochrane (Cochrane Library), Scopus (Elsevier), CINAHL (EBSCOhost), and Embase (Ovid) were conducted. To be included in this scoping review, studies were to be published in a peer reviewed scientific journal, focused on a non-pharmacological lifestyle intervention (physical activity, exercise, sleep, diet, or a combination), and written in English. Forty-one studies were included for analysis. Included participants were predominantly female, living with relapsing-remitting MS, with a median age of 48.3 years. The design of the studies comprised mainly of randomised control trials and pilot/feasibility studies. All included studies incorporated a physical activity intervention, with most examining aerobic/endurance exercise. Most studies reported an effect on improving physical/motor fatigue and a large proportion incorporated an endurance training program. To build on the current evidence and progress MS-fatigue related recommendations, further studies with larger sample sizes and a more inclusive range of MS types are required. Finally, with a gap of research investigating the role of diet and sleep on motor and physical fatigue in MS, research into this field is critically needed.

Several studies indicate that fructose can be used as an energy source for subterranean rodents. However, how subterranean rodents utilize fructose metabolism with no apparent physiological drawbacks remains poorly understood. In the present study, we measured field excitatory postsynaptic potentials (fEPSPs) in hippocampal slices from Gansu zokor and SD rats hippocampi before and 60 min after replacement of 10 mM glucose in the artificial cerebrospinal fluid (ACSF) with 10 mM fructose (gassed with 95 % O₂ and 5 % CO₂). Subsequently, we performed transcriptome analysis on Gansu zokor brains incubated with ACSF containing 10 mM fructose and determined the contents of fructose, lactate, ATP, and UA. Whole brain RNA and proteins were extracted to detect the transcriptional levels of Glut5, Khk, Aldoc, and Cs and the translational levels of GLUT5, CS, NRF2, and c-FOS. The results showed that Gansu zokor brains exhibit higher levels of GLUT5 protein and Khk mRNA levels than SD rats to facilitate fructose uptake and metabolism, resulting in increased fructose, ATP, and lactate content in the brain during fructose incubation. Stable UA levels during fructose metabolism reduce the risk of oxidative stress and neuroinflammation, and activation of the Nrf2 pathway increases downstream antioxidant capacity, thereby reducing brain damage. Persistent fEPSP signaling suggests that fructose supports excitatory synaptic transmission in the CA1 region of the hippocampus of the Gansu zokor but leads to hippocampal dysfunction in SD rats. The unique insights about fructose metabolism in the brain of Gansu zokor obtained in our study will be useful for further studies on the evolution of subterranean rodents.

The human brain possesses the ability to automatically extract statistical regularities from environmental inputs, including visual-graphic symbols and printed units. However, the specific brain regions underlying the statistical learning of these visual-graphic symbols or artificial orthography remain unclear. This study utilized functional magnetic resonance imaging (fMRI) with an artificial orthography learning paradigm to measure brain activities associated with the statistical learning of radical positional regularities embedded in pseudocharacters containing high (100%), moderate (80%), and low (60%) levels of consistency, along with a series of random abstract figures. Thirty adults passively viewed a continuous stream of these pseudocharacters. fMRI data revealed that the left occipital area and the visual word form area (VWFA) exhibited greater responses at the low consistency level than at the high and moderate levels, suggesting implicit statistical learning of positional regularities. Functional connectivity analysis further revealed significant correlations between the occipital lobe, the VWFA, and other brain regions, such as the middle temporal gyrus (MTG), the superior occipital gyrus (SOG), and the cerebellum. Moreover, neural activity showed a tendency to correlate with behavioural recognition performance. These findings demonstrate that the incidental acquisition of statistical regularities in artificial orthography arises from the coordinated activation of multiple distinct neural circuits.

Occlusal tactile acuity (OTA) and bite force are essential components of the sensorimotor control of oral behaviors. While these variables have been studied independently, it has not yet been revealed whether compressive force impacts the occlusal perception mediated by the mechanoreceptive afferents in the periodontal ligament. The present study examined the effect of repetition and maximum bite force on OTA by testing nine aluminum foils of different thicknesses together with a sham test with no foil, three times each, in randomized order in 36 healthy individuals. In addition, the 40 μm foil was tested three more times at the start of each session to evaluate possible short-term effects. This test session was repeated with and without an interspersed maximum bite force task in between. The results demonstrated that repeated measurements increased OTA significantly (p = 0.033); a change mainly driven by the 40 μm thickness, whereas maximum bite force tests did not affect OTA (p = 0.097). Collectively, the results suggest that the enhanced OTA may be attributed to repetition-mediated learning and neuroplasticity within the pathways related to OTA. Furthermore, the compressive bite force may have induced a short-term change that lasted seconds and was not detected by the subsequent OTA measurements or may have altogether inhibited the facilitatory effect of repeated OTA. This underscores the potential for future research to explore the implications of compressive force and pain on OTA in patient populations, which could provide valuable insights into the adaptive mechanisms of the sensorimotor system in pathological conditions.

Neurological disorders significantly impact the central nervous system, contributing to a growing public health crisis globally. The spectrum of these disorders includes neurodevelopmental and neurodegenerative diseases. This manuscript reviews the crucial roles of cellular signalling pathways in the pathophysiology of these conditions, focusing primarily on glutaminase/glutamate/NMDA receptor signalling, alongside the mitogen-activated protein kinase (MAPK) pathways-ERK1/2, C-JNK, and P38 MAPK. Activation of these pathways is often correlated with neuronal excitotoxicity, apoptosis, and inflammation, leading to many other pathological conditions such as traumatic brain injury, stroke, and brain tumor. The interplay between glutamate overstimulation and MAPK signalling exacerbates neurodegenerative processes, underscoring the complexity of cellular communication in maintaining neuronal health. Dysfunctional signalling alters synaptic plasticity and neuronal survival, contributing to cognitive impairments in various neurological diseases. The manuscript emphasizes the potential of targeting these signalling pathways for therapeutic interventions, promoting neuroprotection and reducing neuroinflammation. Incorporating insights from precision medicine and innovative drug delivery systems could enhance treatment efficacy. Overall, understanding the intricate mechanisms of these pathways is essential for developing effective strategies to mitigate the impact of neurological disorders and improve patient outcomes. This review highlights the necessity for further exploration into these signalling cascades to facilitate advancements in therapeutic approaches, ensuring better prognoses for individuals affected by neurological conditions.

Neurological disorders, including cerebral vascular occlusions and strokes, present a major global health challenge due to their high mortality rates and long-term disabilities. Early diagnosis, particularly within the first hours, is crucial for preventing irreversible damage and improving patient outcomes. Although neuroimaging techniques like magnetic resonance imaging (MRI) have advanced significantly, traditional methods often fail to fully capture the complexity of brain lesions. Deep learning has recently emerged as a powerful tool in medical imaging, offering high accuracy in detecting and segmenting brain anomalies. This review examines 61 MRI-based studies published between 2020 and 2024, focusing on the role of deep learning in diagnosing cerebral vascular occlusion-related conditions. It evaluates the successes and limitations of these studies, including the adequacy and diversity of datasets, and addresses challenges such as data privacy and algorithm explainability. Comparisons between convolutional neural network (CNN)-based and Vision Transformer (ViT)-based approaches reveal distinct advantages and limitations. The findings emphasize the importance of ethically secure frameworks, the inclusion of diverse datasets, and improved model interpretability. Advanced architectures like U-Net variants and transformer-based models are highlighted as promising tools to enhance reliability in clinical applications. By automating complex neuroimaging tasks and improving diagnostic accuracy, deep learning facilitates personalized treatment strategies. This review provides a roadmap for integrating technical advancements into clinical practice, underscoring the transformative potential of deep learning in managing neurological disorders and improving healthcare outcomes globally.

Lead (Pb) is an environmental toxin ubiquitously present in the human environment due to anthropogenic activities and industrialization. Lead can enter the human body through various sources and pathways, such as inhalation, ingestion and dermal contact, leading to detrimental health effects. The majority of lead that enters the body is removed by urine or feces; however, under chronic exposure conditions, lead is not efficient, as lead is absorbed and transferred to numerous organs, such as the brain, liver, kidney, muscles, and heart, and it is ultimately stored in mineralizing tissues such as bones and teeth. The central nervous system is the most affected among all the organs and systems affected, as lead is a known neurotoxin. Lead absorption is elevated in the fasting state than in the fed state. Chelation therapy, which is used to treat lead poisoning, has various adverse effects, making this treatment detrimental because it disrupts the levels of other essential elements and redistributes lead to various tissues. One of the main mechanisms by which lead induces toxicity is through the generation of reactive oxygen species. Hence, bioactive compounds that are the source of antioxidants if consumed along with ongoing lead exposure can ameliorate the toxic effects of lead.