Nervous System Function Research Articles

Autonomic biosignals, seizure detection, and forecasting.

Wearable devices have attracted significant attention in epilepsy research in recent years for their potential to enhance patient care through improved seizure monitoring and forecasting. This narrative review presents a detailed overview of the current clinical state of the art while addressing how devices that assess autonomic nervous system (ANS) function reflect seizures and central nervous system (CNS) state changes. This includes a description of the interactions between the CNS and the ANS, including physiological and epilepsy-related changes affecting their dynamics. We first discuss technical aspects of measuring autonomic biosignals and considerations for using ANS sensors in clinical practice. We then review recent seizure detection and seizure forecasting studies, highlighting their performance and capability for seizure detection and forecasting using devices measuring ANS biomarkers. Finally, we address the field's challenges and provide an outlook for future developments.

Sex-dependent effects of carbohydrate source and quantity on caspase-1 activity in the mouse central nervous system

BackgroundMounting evidence links glucose intolerance and diabetes as aspects of metabolic dysregulation that are associated with an increased risk of developing dementia. Inflammation and inflammasome activation have emerged as a potential link between these disparate pathologies. As diet is a key factor in both the development of metabolic disorders and inflammation, we hypothesize that long term changes in dietary factors can influence nervous system function by regulating inflammasome activity and that this phenotype would be sex-dependent, as sex hormones are known to regulate metabolism and immune processes.Methods5-week-old male and female transgenic mice expressing a caspase-1 bioluminescent reporter underwent cranial window surgeries and were fed control (65% complex carbohydrates, 15% fat), high glycemic index (65% carbohydrates from sucrose, 15% fat), or ketogenic (1% complex carbohydrates, 79% fat) diet from 6 to 26 weeks of age. Glucose regulation was assessed with a glucose tolerance test following a 4-h morning fast. Bioluminescence in the brain was quantified using IVIS in vivo imaging. Blood cytokine levels were measured using cytokine bead array. 16S ribosomal RNA gene amplicon sequencing of mouse feces was performed to assess alterations in the gut microbiome. Behavior associated with these dietary changes was also evaluated.ResultsThe ketogenic diet caused weight gain and glucose intolerance in both male and female mice. In male mice, the high glycemic diet led to increased caspase-1 biosensor activation over the course of the study, while in females the ketogenic diet drove an increase in biosensor activation compared to their respective controls. These changes correlated with an increase in inflammatory cytokines present in the serum of test mice and the emergence of anxiety-like behavior. The microbiome composition differed significantly between diets; however no significant link between diet, glucose tolerance, or caspase-1 signal was established.ConclusionsOur findings suggest that diet composition, specifically the source and quantity of carbohydrates, has sex-specific effects on inflammasome activation in the central nervous system and behavior. This phenotype manifested as increased anxiety in male mice, and future studies are needed to determine if this phenotype is linked to alterations in microbiome composition.

Distributed real-time control architecture for electrohydraulic humanoid robots

PurposeThis paper aims to develop an adaptable control architecture for electrohydraulic humanoid robots (HYDROïD) that emulate the functionality of the human nervous system. The developed control architecture overcomes the limitations of classical centralized and decentralized systems by distributing intelligence across controllers.Design/methodology/approachThe proposed solution is a distributed real-time control architecture with robot operating system (ROS). The joint controllers have the intelligence to make decisions, dominate their actuators and publish their state. The real-time capabilities are ensured in the master controller by using a Preempt-RT kernel beside open robot control software middleware to operate the real-time tasks and in the customized joint controllers by free real-time operating systems firmware. Systems can be either centralized, where all components are connected to a central unit or decentralized, where distributed units act as interfaces between the I/Os and the master controller when the master controller is without the ability to make decisions.FindingsThe proposed architecture establishes a versatile and adaptive control framework. It features a centralized hardware topology with a master PC and distributed joint controllers, while the software architecture adapts based on the task. It operates in a distributed manner for precise, force-independent motions and in a decentralized manner for tasks requiring compliance and force control. This design enables the examination of the sensorimotor loop at both low-level joint controllers and the high-level master controller.Originality/valueIt developed a control architecture emulating the functionality of the human nervous system. The experimental validations were performed on the HYDROïD. The results demonstrated 50% advancements in the update rate compared to other humanoids and 30% in the latency of the master processor and the control tasks.

Association of Dietary Retinol Intake and Serum Neurofilament Light Chain Levels: Results from NHANES 2013-2014.

There is increasing evidence suggesting that serum neurofilament light chain (sNfL) levels can be used as biomarkers for axonal injury. Retinol is recognized for its significant involvement in nervous system function, but the precise connection between dietary retinol and sNfL levels remains uncertain. Our objective was to investigate the relationship between dietary retinol intake and sNfL, and to find an optimal retinol intake level for neurological health. In the National Health and Nutrition Examination Survey (NHANES), conducted from 2013 to 2014, a cohort of 1684 participants who met the criteria were selected for the study. sNfL levels were measured from stored serum samples using a novel high-throughput immunoassay platform from Siemens Healthineers. Assessment of dietary retinol intake was performed by a uniformly trained interviewer through a 24 h dietary recall method. A generalized linear model was evaluated to assess the correlation between dietary retinol intake and sNfL concentrations. Furthermore, the nonlinear association between the two is further explored using restricted cubic spline (RCS) analysis. Upon adjusting for potential confounders, a 10% increase in dietary retinol intake was associated with a 3.47% increase in sNfL levels (95% CI: 0.54%, 6.49%) across all participants. This relationship was more pronounced in specific subgroups, including those under 60 years of age, non-obese, impaired estimated glomerular filtration rate (eGFR), and non-diabetic. In subgroup analysis, among those younger than 60 years of age (percent change: 3.80%; 95% CI: 0.43%, 7.28%), changes were found in non-obese participants (percent change: 6.28%; 95% CI: 2.66%, 10.02%), those with impaired eGFR (percent change: 6.90%; 95% CI: 1.44%, 12.65%), and non-diabetic patients (percentage change: 4.17%; 95% CI: 1.08%, 7.36%). RCS analysis showed a linear relationship between dietary retinol intake and sNfL levels. Furthermore, the positive correlation between the two was more significant after the inflection point, according to piecewise linear analysis. This current investigation uncovered a J-shaped relationship between dietary retinol and sNfL levels, suggesting that axonal damage can occur when dietary retinol intake increases more than a specific threshold. These findings need to be further confirmed in future prospective studies to determine the precise intake level that may trigger axonal injury.

ERNEST COST action overview on the (patho)physiology of GPCRs and orphan GPCRs in the nervous system.

G protein-coupled receptors (GPCRs) are a large family of cell surface receptors that play a critical role in nervous system function by transmitting signals between cells and their environment. They are involved in many, if not all, nervous system processes, and their dysfunction has been linked to various neurological disorders representing important drug targets. This overview emphasises the GPCRs of the nervous system, which are the research focus of the members of ERNEST COST action (CA18133) working group 'Biological roles of signal transduction'. First, the (patho)physiological role of the nervous system GPCRs in the modulation of synapse function is discussed. We then debate the (patho)physiology and pharmacology of opioid, acetylcholine, chemokine, melatonin and adhesion GPCRs in the nervous system. Finally, we address the orphan GPCRs, their implication in the nervous system function and disease, and the challenges that need to be addressed to deorphanize them.

Emerging Roles of Microglia in Blood-Brain Barrier Integrity in Aging and Neurodegeneration.

The blood-brain barrier (BBB) is a highly selective interface between the blood and the brain parenchyma. It plays an essential role in maintaining a specialized environment for central nervous system function and homeostasis. The BBB disrupts with age, which contributes to the development of many age-related disorders due to central and peripheral toxic factors or BBB dysfunction. Microglia, the resident innate immune cells of the brain, have recently been explored for their ability to directly and indirectly regulate the integrity of the BBB. This review will focus on the current understanding of the molecular mechanisms utilized by microglia to regulate BBB integrity and how this becomes disrupted in aging and age-associated diseases. We will also discuss the rationale for considering microglia as a therapeutic target to prevent or slow down neurodegeneration.

Parkinson's Disease and Mitotherapy-Based Approaches towards α-Synucleinopathies.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta region of the midbrain and the formation of intracellular protein aggregates known as Lewy bodies, of which a major component is the protein α-synuclein. Several studies have suggested that mitochondria play a central role in the pathogenesis of PD, encompassing both familial and sporadic forms of the disease. Mitochondrial dysfunction is attributed to bioenergetic impairment, increased oxidative stress, damage to mitochondrial DNA, and alteration in mitochondrial morphology. These alterations may contribute to improper functioning of the central nervous system and ultimately lead to neurodegeneration. The perturbation of mitochondrial function makes it a potential target, worthy of exploration for neuroprotective therapies and to improve mitochondrial health in PD. Thus, in the current review, we provide an update on mitochondria-based therapeutic approaches toward α-synucleinopathies in PD.

Neurodegenerative Diseases: Unraveling the Heterogeneity of Astrocytes.

The astrocyte population, around 50% of human brain cells, plays a crucial role in maintaining the overall health and functionality of the central nervous system (CNS). Astrocytes are vital in orchestrating neuronal development by releasing synaptogenic molecules and eliminating excessive synapses. They also modulate neuronal excitability and contribute to CNS homeostasis, promoting neuronal survival by clearance of neurotransmitters, transporting metabolites, and secreting trophic factors. Astrocytes are highly heterogeneous and respond to CNS injuries and diseases through a process known as reactive astrogliosis, which can contribute to both inflammation and its resolution. Recent evidence has revealed remarkable alterations in astrocyte transcriptomes in response to several diseases, identifying at least two distinct phenotypes called A1 or neurotoxic and A2 or neuroprotective astrocytes. However, due to the vast heterogeneity of these cells, it is limited to classify them into only two phenotypes. This review explores the various physiological and pathophysiological roles, potential markers, and pathways that might be activated in different astrocytic phenotypes. Furthermore, we discuss the astrocyte heterogeneity in the main neurodegenerative diseases and identify potential therapeutic strategies. Understanding the underlying mechanisms in the differentiation and imbalance of the astrocytic population will allow the identification of specific biomarkers and timely therapeutic approaches in various neurodegenerative diseases.

Advances in the application of fecal microbiota transplantation for the treatment of nervous system diseases

The intestinal microbiota exhibits a strong correlation with the function of the central nervous system, exerting influence on the host brain through neural pathways, immune pathways, and microbial metabolites along the gut-brain axis. Disorders in the composition of the intestinal microbial are closely associated with the onset and progression of neurological disorders, such as depression, Alzheimer's disease, and Parkinson's disease. It has been proven that fecal microbiota transplantation can improve symptoms in animal models of neurological diseases and clinical patients. This paper provides a comprehensive review of the composition and function of the human intestinal microbiota, as well as the intricate the relationship between the human intestinal microbiota and nervous system diseases through the gut-brain axis. Additionally, it delves into the research advancements and underlying mechanism of fecal microbiota transplantation in the treatment of nervous system diseases. These findings offer novel insights and potential avenues for clinical interventions targeting nervous system diseases.

The associations among glycemic control, heart variability, and autonomic brain function in healthy individuals: Age- and sex-related differences

IntroductionThe purpose of this study was to clarify the relationships between glycemia and function of the autonomic nervous system (ANS), assessed via resting-state functional connectivity (FC) and heart-rate variability (HRV). MethodsData for this study were extracted from the Leipzig Study for Mind-Body-Emotion Interactions, including 146 healthy adults (114 young, 32 older). Variables of interest were glycated hemoglobin (HbA1c), resting-state FC in the salience aspect of the central-autonomic (S-CAN) and salience network (SN) and HRV (RMSSD and high-frequency HRV (HF-HRV)). ResultsHbA1c was inversely correlated with FC in the S-CAN but not SN. HbA1c was inversely correlated with HRV. Both RMSSD and log(HF-HRV) were correlated with FC in the S-CAN and SN. Age- (not sex-related) differences were observed in the Hb1Ac-FC associations (stronger in older adults) while sex- (not age-related) differences were observed in the HRV-FC (stronger in females). ConclusionsThese findings extend the diabetes literature to healthy adults in relating glycemia and brain function. The age- and sex-related differences in these relationships highlight the need to account for the potential effects of age and sex in future investigations.

Analysis of fetal heart rate fluctuations in women diagnosed with preeclampsia during the latent phase of labor

IntroductionFetal heart rate variability (fHRV) is a tool used to investigate the functioning of the fetal autonomic nervous system. Despite the significance of preeclampsia, fHRV during the latent phase of labor has not been extensively studied. This study aimed to evaluate fetal cardiac autonomic activity by using linear and nonlinear indices of fHRV analysis in women diagnosed with preeclampsia without hypertensive treatment during gestation, compared to normotensive women during the latent phase of labor.MethodsA cross-sectional and exploratory study was conducted among pregnant women in the latent phase of labor, forming three study groups: normotensive or control (C, 38.8 ± 1.3 weeks of pregnancy, n = 22), preeclampsia with moderate features (P, 37.6 ± 1.4 weeks of pregnancy n = 10), and preeclampsia with severe features (SP, 36.9 ± 1.2 weeks of pregnancy, n = 12). None of the participants received anti-hypertensive treatment during their pregnancy. Linear and nonlinear features of beat-to-beat fHRV, including temporal, frequency, symbolic dynamics, and entropy measures, were analyzed to compare normotensive and preeclamptic groups.ResultsSignificantly lower values of multiscale entropy (MSE) and short-term complexity index (Ci) were observed in the preeclamptic groups compared to the C group (p < 0.05). Additionally, higher values of SDNN (standard deviation of R-R intervals) and higher values of low-frequency power (LF) were found in the P group compared to the C group.ConclusionOur findings indicate that changes in the complexity of fetal heart rate fluctuations may indicate possible disruptions in the autonomic nervous system of fetuses in groups affected by undiagnosed preeclampsia during pregnancy. Reduced complexity and shifts in fetal autonomic cardiac activity could be associated with preeclampsia’s pathophysiological mechanisms during the latent phase of labor.

Vestibular Function is Associated with Prefrontal and Sensorimotor Cortical Gray Matter Volumes in a Cross-Sectional Study of Healthy, Older Adults

Background The vestibular system is associated with alterations in the structure and function of the central nervous system. Yet, whether age-related vestibular loss is related to volume loss in the cerebral cortical areas that have been reported to receive vestibular input remains unknown. In this cross-sectional study of 117 healthy, older adults from the Baltimore Longitudinal Study of Aging, we examine the relationships between age-related vestibular functions and the gray matter volumes of the prefrontal cortex and its subregions and of the sensorimotor cortex—regions known to process vestibular information. Methods T1-weighted MRI scans were automatically segmented using MRICloud. Log-linear multiple regression was used to investigate the relationships between average regional volume and vestibular function, adjusting for age, sex, and intracranial volume. Permutation testing was used for hypothesis testing, and bootstrapping was used to estimate confidence intervals. Results We found that age-related changes in vestibular end-organ function are associated with differentially altered gray matter volumes in the prefrontal and sensorimotor cortices, with many findings persisting when considering left (or right) side only. Concomitant with age-related, global brain atrophy, lower canal and utricular function were associated with additional volume atrophy of the prefrontal cortex and middle frontal gyrus, respectively. Lower saccular and utricular function were associated with the preservation of the volumes of the sensorimotor cortex and the pole of the superior frontal gyrus, respectively, against age-related, global brain atrophy. Canal and utricular function were not associated with the volumes of the sensorimotor cortex, and saccular function was not associated with the relative volumes of the prefrontal cortex. Conclusion Together, these findings of relative volume preservation or additional atrophy suggest that vestibular function may play a role in the resilience to or magnification of global age effects on cerebral cortical structure.

#2368 GHRH levels and AhR expression in CKD patients before and after kidney transplantation

Abstract Background and Aims Chronic kidney disease (CKD) is an irreversible decline in renal function where kidney transplantation (KT) is the optimal therapeutic intervention. We aim to investigate the role and activation of the uremic toxin receptor aryl hydrocarbon receptor (AhR) in the microvasculature, particularly its implication in the blood-brain barrier impairment. We will also explore the potential role of growth hormone-releasing hormone (GHRH) as a biomarker reflecting the resolution of uremia-induced inflammation, early vascular ageing (EVA) phenotype, and potential enhancement in central nervous system (CNS) function post-KT. Method Resistance arteries from KT patients and non-CKD controls were isolated and expression of AhR was analysed by immunohistochemistry. The study used plasma samples from 60 KT patients, and levels of GHRH were measured at baseline and two years after transplantation using ELISA. Results Following KT, our initial findings indicate a decrease in levels of DBP, Lp(a), creatinine, homocysteine, phosphate, and troponin T among KT patients. Conversely, there was an increase in albumin, HBA1c, calcium and NfL post-transplantation. The expression of AhR in the resistance arteries of KT patients (2.6%) was notably lower compared to non-CKD controls (9.7%). Plasma concentrations of GHRH were significantly higher (p < 0.0001) in CKD-5 patients two years post-KT (2.94 ng/mL, IQR 2.60-3.43) compared to baseline (2.32 mg/L, IQR 1.84-3.24). This elevated trend in GHRH levels post-KT was observed in both sexes, with males (p < 0.0001) and females (p 0.0084) showing higher levels—males (3.0 ng/mL, IQR 2.6-3.5) and females (2.8 ng/mL, IQR 2.4-3.5)—compared to baseline level of males (2.4 ng/mL, IQR 1.8-3.2) and females (2.2 ng/mL, 1.9-3.3). No significant difference in GHRH levels was observed when assessing extreme EVA phenotypes based on the presence or absence of calcification or fibrosis. Conclusion Contrary to our initial expectation, the preliminary results indicate a downregulation in AhR expression within resistance vessels of CKD patients, implying modifications in AhR signaling within the uremic environment. The observed alteration in GHRH levels presents a promising avenue for further investigation focusing on its possible application as a biomarker for assessing CNS status in CKD patients undergoing KT. Prospective clinical application could involve the administration of GHRH agonists as a protective measure against cognitive impairment, considering its deficiency in CKD. Such supplementation holds promise to prevent further cognitive morbidity. The modulation in the levels of this hormone has the potential to significantly influence the treatment trajectory of CKD patients and enhance clinical outcomes.

Kainate receptor channel opening and gating mechanism

Kainate receptors, a subclass of ionotropic glutamate receptors, are tetrameric ligand-gated ion channels that mediate excitatory neurotransmission1–4. Kainate receptors modulate neuronal circuits and synaptic plasticity during the development and function of the central nervous system and are implicated in various neurological and psychiatric diseases, including epilepsy, depression, schizophrenia, anxiety and autism5–11. Although structures of kainate receptor domains and subunit assemblies are available12–18, the mechanism of kainate receptor gating remains poorly understood. Here we present cryo-electron microscopy structures of the kainate receptor GluK2 in the presence of the agonist glutamate and the positive allosteric modulators lectin concanavalin A and BPAM344. Concanavalin A and BPAM344 inhibit kainate receptor desensitization and prolong activation by acting as a spacer between the amino-terminal and ligand-binding domains and a stabilizer of the ligand-binding domain dimer interface, respectively. Channel opening involves the kinking of all four pore-forming M3 helices. Our structures reveal the molecular basis of kainate receptor gating, which could guide the development of drugs for treatment of neurological disorders.

Unraveling the Intricacies of OPG/RANKL/RANK Biology and Its Implications in Neurological Disorders-A Comprehensive Literature Review.

The OPG/RANKL/RANK framework, along with its specific receptors, plays a crucial role in bone remodeling and the functioning of the central nervous system (CNS) and associated disorders. Recent research and investigations provide evidence that the components of osteoprotegerin (OPG), receptor activator of NF-kB ligand (RANKL), and receptor activator of NF-kB (RANK) are expressed in the CNS. The CNS structure encompasses cells involved in neuroinflammation, including local macrophages, inflammatory cells, and microglia that cross the blood-brain barrier. The OPG/RANKL/RANK trio modulates the neuroinflammatory response based on the molecular context. The levels of OPG/RANKL/RANK components can serve as biomarkers in the blood and cerebrospinal fluid. They act as neuroprotectants following brain injuries and also participate in the regulation of body weight, internal body temperature, brain ischemia, autoimmune encephalopathy, and energy metabolism. Although the OPG/RANKL/RANK system is primarily known for its role in bone remodeling, further exploring deeper into its multifunctional nature can uncover new functions and novel drug targets for diseases not previously associated with OPG/RANKL/RANK signaling.

Metal toxicity exposure in Alzheimer's disease - literature review

Introduction and purpose: As the elderly population grows, the risk of cognitive decline and dementia increases. Environmental toxicants, including metals, have been identified as potential contributors to these conditions. This literature review investigated the potential contribution of metals, such as aluminium, lead, zinc and copper to Alzheimer's disease development.Material and methods: The literature was conducted using "Pub Med" and "Google Scholar" databases with the keywords "metals", "Alzheimer's disease", "aluminium", "lead", "neurodegenerative diseases", "copper".Brief description of the state of knowledge: Metals can negatively affect the functionality of the central nervous system, leading to impairments in behavior, motor skills, and cognitive abilities. The development of Alzheimer's disease can be influenced by several factors, including Aβ aggregates, tau tangles, synaptic dysfunction, inflammation, and oxidative stress, which may be worsened by interactions with these metals.Results and conclusions: Extensive research has shown a link between metal exposure and neurodegeneration. Understanding the role of metals like lead, copper, aluminum, and zinc in Alzheimer's disease pathogenesis remains crucial, but further investigation is needed. A better insight into the impact of metal exposure on brain health could help find the way for effective prevention and treatment strategies for neurodegenerative diseases.

Timing-dependent synergies between motor cortex and posterior spinal stimulation in humans.

Volitional movement requires descending input from the motor cortex and sensory feedback through the spinal cord. We previously developed a paired brain and spinal electrical stimulation approach in rats that relies on convergence of the descending motor and spinal sensory stimuli in the cervical cord. This approach strengthened sensorimotor circuits and improved volitional movement through associative plasticity. In humans, it is not known whether posterior epidural spinal cord stimulation targeted at the sensorimotor interface or anterior epidural spinal cord stimulation targeted within the motor system is effective at facilitating brain evoked responses. In 59 individuals undergoing elective cervical spine decompression surgery, the motor cortex was stimulated with scalp electrodes and the spinal cord was stimulated with epidural electrodes, with muscle responses being recorded in arm and leg muscles. Spinal electrodes were placed either posteriorly or anteriorly, and the interval between cortex and spinal cord stimulation was varied. Pairing stimulation between the motor cortex and spinal sensory (posterior) but not spinal motor (anterior) stimulation produced motor evoked potentials that were over five times larger than brain stimulation alone. This strong augmentation occurred only when descending motor and spinal afferent stimuli were timed to converge in the spinal cord. Paired stimulation also increased the selectivity of muscle responses relative to unpaired brain or spinal cord stimulation. Finally, clinical signs suggest that facilitation was observed in both injured and uninjured segments of the spinal cord. The large effect size of this paired stimulation makes it a promising candidate for therapeutic neuromodulation. KEY POINTS: Pairs of stimuli designed to alter nervous system function typically target the motor system, or one targets the sensory system and the other targets the motor system for convergence in cortex. In humans undergoing clinically indicated surgery, we tested paired brain and spinal cord stimulation that we developed in rats aiming to target sensorimotor convergence in the cervical cord. Arm and hand muscle responses to paired sensorimotor stimulation were more than five times larger than brain or spinal cord stimulation alone when applied to the posterior but not anterior spinal cord. Arm and hand muscle responses to paired stimulation were more selective for targeted muscles than the brain- or spinal-only conditions, especially at latencies that produced the strongest effects of paired stimulation. Measures of clinical evidence of compression were only weakly related to the paired stimulation effect, suggesting that it could be applied as therapy in people affected by disorders of the central nervous system.

Significance of the Gut-Brain Axis in the Development of Overweight and Obesity

Introduction: The global obesity crisis results from inactive lifestyles and poor diets, increasing the risk of metabolic disorders. Emerging research links obesity with gut microbiome changes influenced by factors like age, genetics, and diet. Gut-brain communication via neural, endocrine, and inflammatory pathways, influenced by microbial compounds, affects nervous system function. Materials and Methods of Research: A thorough literature review was performed using PubMed and Google Scholar, employing keywords related to the gut-brain axis and obesity. Results: Obesity shifts gut microbiota composition due to factors like childbirth method, diet, antibiotics, and environment. This imbalance impacts metabolism, appetite, and insulin sensitivity. Gut microbes influence the brain, regulating energy balance and inflammation. Dysregulated tryptophan metabolism leads to insulin resistance. Gut-brain communication via the vagal nerve affects nutrient metabolism. Hormones like insulin and leptin, along with microbial metabolites, affect lipid metabolism and appetite. Gut microbiota abundance correlates with leptin signaling, and changes in ghrelin levels relate to microbiota composition. Microbial presence affects food cravings. Inflammation in obesity is linked to gut microbiota changes, mediated by bile acids and microbial metabolites. Interventions like probiotics and fecal microbiota transplantation offer potential for managing obesity. Emerging therapies like peptide D3 hold promise but require further study. Conclusion: The microbiome-gut-brain axis is vital in obesity, affecting metabolism, inflammation, and appetite. Utilizing interventions such as dietary adjustments and probiotics targeting gut-brain signaling shows promise in managing obesity. Personalized approaches are crucial due to microbiome complexity. Further research is needed to develop effective therapies for the obesity epidemic.

How AI originates from biology – and how it returns to it

The most popular types of artificial intelligence are inspired by different biological processes, such as the functioning of nervous systems or adaptive immunity. Here, I make a short dive into the history of AI to track how bio-inspired models of AI replace other models and discuss which model could be the next one.

Amino acid transporters in neurological disorders and neuroprotective effects of cysteine derivatives

For most diseases and disorders occurring in the brain, the full causes behind them are yet unknown, but many show signs of dysfunction of amino acid transporters or abnormalities in amino acid metabolism. The blood-brain barrier (BBB) plays a key role in supporting the function of the central nervous system (CNS). Because of its unique structure, the BBB can maintain the optimal environment for CNS by controlling the passage of hydrophilic molecules from blood to the brain. Nutrients, such as amino acids, can cross the BBB via specific transporters. Many amino acids are essential for CNS function, and dysfunction of these amino acid transporters can lead to abnormalities in amino acid levels. This has been linked to causes behind certain genetic brain diseases, such as schizophrenia, autism spectrum disorder, and Huntington's disease (HD). One example of crucial amino acids is L-Cys, the rate-limiting factor in the biosynthesis of an important antioxidant, glutathione (GSH). Deficiency of L-Cys and GSH has been linked to oxidative stress and has been shown as a plausible cause behind certain CNS diseases, like schizophrenia and HD. This review presents the current status of potential L-Cys therapies and gives future directions that can be taken to improve amino acid transportation related to distinct CNS diseases.