Search Results (65)

Smart devices and multimodal biosignal systems, including electroencephalography (EEG/MEG), ECG-derived heart rate variability (HRV), and electromyography (EMG), increasingly supported by artificial intelligence (AI), are being explored to improve the assessment and longitudinal monitoring of mental health conditions. Despite rapid growth, the available evidence remains heterogeneous, and clinical translation is limited by variability in acquisition protocols, analytical pipelines, and validation quality. This systematic review synthesizes current applications, signal-processing approaches, and methodological limitations of biosignal-based smart systems for mental health monitoring. Methods: A PRISMA 2020-guided systematic review was conducted across PubMed/MEDLINE, Scopus, the Web of Science Core Collection, IEEE Xplore, and the ACM Digital Library for studies published between 2013 and 2026. Eligible records reported human applications of wearable/smart devices or multimodal biosignals (e.g., EEG/MEG, ECG/HRV, EMG, EDA/GSR, and sleep/activity) for the detection, monitoring, or management of mental health outcomes. The reviewed literature after predefined inclusion/exclusion criteria clustered into six themes: depression detection and monitoring (37%), stress/anxiety management (18%), post-traumatic stress disorder (PTSD)/trauma (5%), technological innovations for monitoring (25%), brain-state-dependent stimulation/interventions (3%), and socioeconomic context (7%). Across modalities, common analytical pipelines included artifact suppression, feature extraction (time/frequency/nonlinear indices such as entropy and complexity), and machine learning/deep learning models (e.g., SVM, random forests, CNNs, and transformers) for classification or prediction. However, 67% of studies involved sample sizes below 100 participants, limited ecological validity, and lacked external validation; heterogeneity in protocols and outcomes constrained comparability. Conclusions: Overall, multimodal systems demonstrate strong potential to augment conventional mental health assessment, particularly via wearable cardiac metrics and passive sensing approaches, but current evidence is dominated by proof-of-concept studies. Future work should prioritize standardized reporting, rigorous validation in diverse real-world cohorts, transparent model evaluations, and ethics-by-design principles (privacy, fairness, and clinical governance) to support translation into practice. Full article

Background: Aging is traditionally characterized by progressive structural and cognitive decline; however, increasing evidence shows that the aging brain retains a remarkable capacity for reorganization. This adaptive neuroplasticity supports cognitive resilience—defined as the ability to maintain efficient cognitive performance despite age-related neural vulnerability. Objective: To synthesize current molecular, cellular, neuroimaging, and electrophysiological neuromarkers that characterize adaptive neuroplasticity and to examine how these mechanisms contribute to cognitive resilience across aging. Methods: This narrative review integrates findings from molecular neuroscience, multimodal neuroimaging (fMRI, DTI, PET), electrophysiology (EEG, MEG, TMS), and behavioral research to outline multiscale biomarkers associated with compensatory and efficient neural reorganization in older adults. Results: Adaptive neuroplasticity emerges from the coordinated interaction of neurotrophic signaling (BDNF, CREB, IGF-1), glial modulation (astrocytic lactate metabolism, regulated microglial activity), synaptic remodeling, and neurovascular support (VEGF, nitric oxide). Multimodal neuromarkers—including preserved frontoparietal connectivity, DMN–FPCN coupling, synaptic density (SV2A-PET), theta–gamma coherence, and LTP-like excitability—consistently correlate with resilience in executive functions, memory, and processing speed. Behavioral enrichment, physical activity, and cognitive training further enhance these biomarkers, creating a bidirectional loop between experience and neural adaptability. Conclusions: Adaptive neuroplasticity represents a fundamental mechanism through which older adults maintain cognitive function despite biological aging. Integrating molecular, imaging, electrophysiological, and behavioral neuromarkers provides a comprehensive framework to identify resilience trajectories and to guide personalized interventions aimed at preserving cognition. Understanding these multilevel adaptive mechanisms reframes aging not as passive decline but as a dynamic continuum of biological compensation and cognitive preservation. Full article

Gliomas are the most common malignant primary brain tumors in adults. The treatment of high-grade gliomas is very limited due to their diffuse infiltration, high plasticity, and resistance to conventional therapies. Although they were long considered passive massive lesions, they are now regarded as functionally integrated components of neural circuits, as they form authentic electrochemical synapses with neurons. This allows them to mimic neuronal activity to drive tumor growth and invasion. Ultrastructural studies show presynaptic vesicles in neurons and postsynaptic densities in glioma cell membranes, while electrophysiological recordings detect postsynaptic currents in tumor cells. Tumor microtubules (TMs), dynamic cytoplasmic protrusions enriched in AMPA receptors, are the structures responsible for glioma–glioma and glioma–neuron connectivity, also contributing to treatment resistance and tumor network integration. In these connections, neurons release glutamate that mainly activates their AMPA receptors in glioma cells, while gliomas release excess glutamate, causing excitotoxicity, altering the local excitatory-inhibitory balance, and promoting a hyperexcitable and pro-tumorigenic microenvironment. In addition, certain gliomas, such as diffuse midline gliomas, have altered chloride homeostasis, which makes GABAergic signaling depolarizing and growth promoting. Synaptogenic factors, such as neuroligin-3 and BDNF, further enhance glioma proliferation and synapse formation. These synaptic and paracrine interactions contribute to cognitive impairment, epileptogenesis, and resistance to surgical and pharmacological interventions. High functional connectivity within gliomas correlates with shorter patient survival. Therapies such as AMPA receptor antagonists (perampanel), glutamate release modulators (riluzole or sulfasalazine), and chloride cotransporter inhibitors (NKCC1 blockers) aim to improve outcomes for patients. Full article

Microbiome-derived metabolites have emerged as key mediators of the gut–brain axis, influencing cognitive function and neuroprotection. This study investigated whether Lactobacillus delbrueckii subsp. lactis CKDB001 alleviates scopolamine-induced memory impairment through metabolic modulation, and how its effects compare with those of donepezil. ICR mice were administered CKDB001 or donepezil for 4–5 weeks and evaluated through behavioral, microbiome, metabolomic, and molecular analyses. CKDB001 significantly improved spatial working memory in a dose-dependent manner, with the high-dose group showing improvements comparable to those of the donepezil-treated group, while passive avoidance showed a non-significant but positive trend. Both CKDB001 and donepezil modulated gut microbial composition, leading to a partial divergence from the scopolamine-disrupted community structure, with CKDB001 inducing dose-dependent intestinal colonization. Metabolomic profiling revealed that both treatments increased tryptophan-derived indole metabolites and altered lipid and short-chain fatty acid metabolite profiles, although these effects were more pronounced in CKDB001-treated mice. At the molecular level, both CKDB001 and donepezil reduced hippocampal tau phosphorylation, downregulated glycogen synthase kinase-3 (GSK-3) signaling, enhanced intestinal tight-junction proteins, and partially normalized acetylcholinesterase activity, with CKDB001 restoring AChE levels more closely toward the normal control. Together, these findings suggest that CKDB001 mitigates cognitive deficits through coordinated modulation of microbial, metabolic, and neuronal pathways, offering a microbiome-based therapeutic approach that may provide benefits comparable to donepezil with potentially fewer limitations. Full article

Docosahexaenoic acid (DHA), the dominant polyunsaturated fatty acid in photoreceptors, neurons, and synapses, is usually described as a passive structural membrane constituent. We propose a different view: DHA is a quantum-electronically active molecule whose methylene interrupted double-bond system creates an electron-rich matrix that couples with proteins to form quantum “clouds” and high-speed signaling central to recognition, recall, and cognition. Integrating evidence from molecular evolution, biophysics, and neuroscience, we argue that, as the original chromophore, DHA’s unique properties enabled the emergence of the nervous system and continue to provide the electronic substrate for cognition. By suggesting that cognition depends not only on protein-based mechanisms but on DHA-mediated electron dynamics at the membrane–protein interface, this perspective reframes DHA as an active, conserved determinant of brain evolution and function. Full article

Music is a near-universal anthropological and sensory phenomenon that engages distributed brain networks and peripheral physiological systems to shape emotion, cognition, sociality, and bodily regulation. Evidence from electrophysiology, neuroimaging, endocrinology, randomized controlled trials, and longitudinal training studies indicates that both receptive and active musical experiences produce experience-dependent neural and systemic adaptations. These include entrainment of neural oscillations, modulation of predictive and reward signaling, autonomic and neuroendocrine changes, and long-term structural connectivity alterations that support affect regulation, cognition, social functioning, motor control, sleep, and resilience to neuropsychiatric illness. This narrative review integrates mechanistic domains with clinical outcomes across major conditions, such as depression, anxiety, schizophrenia, dementia, and selected neurodevelopmental disorders, by mapping acoustic and procedural parameters onto plausible biological pathways. We summarize how tempo, beat regularity, timbre and spectral content, predictability, active versus passive engagement, social context, dose, and timing influence neural entrainment, synaptic and network plasticity, reward and prediction-error dynamics, autonomic balance, and immune/endocrine mediators. For each condition, we synthesize randomized and observational findings and explicitly link observed improvements to mechanistic pathways. We identify methodological limitations, including heterogeneous interventions, small and biased samples, sparse longitudinal imaging and standardized physiological endpoints, and inconsistent acoustic reporting, and translate these into recommendations for translational trials: harmonized acoustic reporting, pre-specified mechanistic endpoints (neuroimaging, autonomic, neuroendocrine, immune markers), adequately powered randomized designs with active controls, and long-term follow-up. Contextual moderators including music education, socioeconomic and cultural factors, sport, sleep, and ritual practices are emphasized as critical determinants of implementation and effectiveness. Full article

Astrocytic calcium signaling is a central mechanism of neuron-glia communication that operates across multiple spatial and temporal scales. Traditionally, research has focused on intracellular Ca²⁺ oscillations that regulate gliotransmitter release, ion homeostasis, and metabolic support. Recent evidence, however, reveals that extracellular calcium ([Ca²⁺]o) is not a passive reservoir but a dynamic signaling mediator capable of influencing neuronal excitability within milliseconds. Through mechanisms such as calcium-sensing receptor (CaSR) activation, ion channel modulation, surface charge effects, and ephaptic coupling, astrocytes emerge as active partners in both slow and rapid modes of communication. This dual perspective reshapes our understanding of brain physiology and disease. Disrupted Ca²⁺ signaling contributes to network instability in epilepsy, synaptic dysfunction in Alzheimer’s and Parkinson’s disease, and impaired maturation in neurodevelopmental disorders. Methodological advances, including Ca²⁺-selective microelectrodes, genetically encoded extracellular indicators, and computational modeling, are beginning to uncover the richness of extracellular Ca²⁺ dynamics, though challenges remain in achieving sufficient spatial and temporal resolution. By integrating classical intracellular pathways with emerging insights into extracellular signaling, this review highlights astrocytes as central architects of the ionic landscape. Recognizing calcium as both an intracellular messenger and an extracellular signaling mediator provides a unifying framework for neuron–glia interactions and opens new avenues for therapeutic intervention. Full article

Background/Objectives: Polygonatum sibiricum (PS), possessing both medicinal and edible dual functions, boasts a long history of application in Chinese traditional practices. As a component of its effectiveness, Polygonatum sibiricum polysaccharides (PSPs) have been reported to exert neuroprotective effects. However, the protective effects of PS on the cognitive deficits induced by simulated weightlessness remain unclear. This study evaluated the therapeutic potential of PSPs to counteract the cognitive deficits induced by simulated weightlessness using the Hindlimb Unloading (HU) method. Methods: Mice were subjected to HU to establish cognitive impairment, and PSP was administered for four weeks. The Morris water maze test (MWMT) and passive avoidance test (PAT) were used to evaluate the cognitive abilities of mice, followed by an analysis of molecular mechanisms. Results: PSP treatment increased learning and memory in mice. PSP treatment partially restored gut microbial diversity and composition towards beneficial taxa, including Lactobacillus and Firmicutes, while inhibiting proinflammatory genera, including Alistipes and Proteus. At the same time, PSP upregulated Claudin-5 and Zonula Occludens-1 (ZO-1) levels in the colon, suggesting improved intestinal barrier integrity, and decreased neuroinflammatory response by inhibiting NLRP3 inflammasome activation and NF-κB phosphorylation in the hippocampus. It also modulated neurotransmitter homeostasis along the microbiota–gut–brain (MGB) axis by increasing the levels of gamma-aminobutyric acid (GABA) and serotonin (5-HT) while reducing the levels of excitotoxic metabolites, including Glutamate (Glu) and 3-hydroxykynurenine (3-HK). Conclusions: These results indicate that PSP may have beneficial effects on HU-induced cognitive impairment by regulating gut microbiota, enhancing barrier function, suppressing neuroimmune signaling, and restoring neurotransmitter balance. Full article

Decoding motor imagery (MI) of lower-limb movements from electroencephalography (EEG) signals remains a challenge due to the involvement of deep cortical regions, limiting the applicability of Brain–Computer Interfaces (BCIs). This study proposes a novel protocol that combines passive pedaling (PP) as sensory priming with MI at different speeds (30, 45, and 60 rpm) to improve EEG-based classification. Ten healthy participants performed PP followed by MI tasks while EEG data were recorded. An increase in spectral relative power around Cz associated with both PP and MI was observed, varying with speed and suggesting that PP may enhance cortical engagement during MI. Furthermore, our classification strategy, based on Convolutional Neural Networks (CNNs), achieved an accuracy of 0.87–0.89 across four classes (three speeds and rest). This performance was also compared with the standard Common Spatial Patterns (CSP) and Linear Discriminant Analysis (LDA), which achieved an accuracy of 0.67–0.76. These results demonstrate the feasibility of multiclass decoding of imagined pedaling velocities and lay the groundwork for speed-adaptive BCIs, supporting future personalized and user-centered neurorehabilitation interventions. Full article

Alzheimer’s disease is characterized by progressive cognitive decline associated with oxidative stress, neuroinflammation, and impaired neurotrophic signaling. Sulforaphane, a bioactive compound found in broccoli, has demonstrated neuroprotective effects by activating NRF2 and inhibiting NF-κB. However, the efficacy of whole-food-derived sulforaphane remains unclear. This study evaluated the neuroprotective potential of broccoli sprout extract using a scopolamine-induced mouse model of memory impairment. Mice were orally administered broccoli sprout extract once daily at doses of 100 mg/kg or 200 mg/kg for four weeks prior to behavioral and biochemical assessments. Treatment with broccoli sprout extract significantly improved scopolamine-induced deficits in long-term memory, as determined by the passive avoidance test. The spatial working memory remained unaffected. High doses of broccoli sprout extract restored hippocampal brain-derived neurotrophic factor levels and reduced cortical lipid peroxidation, suggesting antioxidant and neurotrophic benefits. Additionally, the low dose preserved striatal choline acetyltransferase expression and reduced systemic tumor necrosis factor-alpha and hippocampal cyclooxygenase-2 levels, indicating its anti-inflammatory and cholinergic protective effects. No significant changes in acetylcholinesterase activity or glutathione levels were observed. Overall, these results imply that broccoli sprout extract has multi-targeted neuroprotective effects, possibly involving redox and inflammatory regulation. Therefore, it may be a safe dietary strategy to support cognition in neurodegenerative conditions. Full article

This review outlines the technological principles of neural–computer interface (NCI) construction, classifying them according to: (1) the degree of intervention (invasive, semi-invasive, and non-invasive); (2) the direction of signal communication, including BCI (brain–computer interface) for converting neural activity into commands for external devices, CBI (computer–brain interface) for translating artificial signals into stimuli for the CNS, and BBI (brain–brain interface) for direct brain-to-brain interaction systems that account for agency; and (3) the mode of user interaction with technology (active, reactive, passive). For each NCI type, we detail the fundamental data processing principles, covering signal registration, digitization, preprocessing, classification, encoding, command execution, and stimulation, alongside engineering implementations ranging from EEG/MEG to intracortical implants and from transcranial magnetic stimulation (TMS) to intracortical microstimulation (ICMS). We also review mathematical modeling methods for NCIs, focusing on optimizing the extraction of informative features from neural signals—decoding for BCI and encoding for CBI—followed by a discussion of quasi-real-time operation and the use of DSP and neuromorphic chips. Quantitative metrics and rehabilitation measures for evaluating NCI system effectiveness are considered. Finally, we highlight promising future research directions, such as the development of electrochemical interfaces, biomimetic hierarchical systems, and energy-efficient technologies capable of expanding brain functionality. Full article

Functional near-infrared spectroscopy (fNIRS) allows non-invasive assessment of cortical activity during naturalistic tasks. This study aimed to compare cortical activation dynamics—specifically the latency (t_max) and amplitude (ΔoxyHb) of oxygenated haemoglobin changes—in passive observation and an interactive task using the Nefroball system. A total of 117 healthy adults performed two tasks involving rhythmic hand movements: a passive protocol and an interactive game-controlled condition. fNIRS recorded signals from the visual, parietal, motor, and prefrontal cortices of the left hemisphere. The Mann–Whitney test revealed significantly shorter t_max in all areas during the interactive task, suggesting faster recruitment of cortical networks. ΔoxyHb amplitude was significantly higher only in the visual cortex during the interactive task, indicating increased visual processing demand. No significant ΔoxyHb differences were observed in the motor, prefrontal, or parietal cortices. Weak but significant positive correlations were found between tmax and ΔoxyHb in the motor and prefrontal regions, but only in the passive condition. These findings support the notion that interactive tasks elicit faster, though not necessarily stronger, cortical responses. The results have potential implications for designing rehabilitation protocols and brain–computer interfaces involving visual–motor integration. Full article

Intracranial pressure (ICP) pulse wave morphology, including the ratios of the three characteristic peaks (P1, P2, and P3), offers valuable insights into intracranial dynamics and brain compliance. Traditional invasive methods for ICP pulse wave monitoring pose significant risks, highlighting the need for non-invasive alternatives. This pilot study investigates a novel non-invasive method for monitoring ICP pulse waves through closed eyelids, using a specially designed, liquid-filled, fully passive sensor system named ‘Archimedes 02’. To our knowledge, this is the first technological approach that enables the non-invasive monitoring of ICP pulse waveforms via closed eyelids. This study involved 10 healthy volunteers, aged 26–39 years, who underwent resting-state non-invasive ICP pulse wave monitoring sessions using the ‘Archimedes 02’ device while in the supine position. The recorded signals were processed to extract pulse waves and evaluate their morphological characteristics. The results indicated successful detection of pressure pulse waves, showing the expected three peaks (P1, P2, and P3) in all subjects. The calculated P2/P1 ratios were 0.762 (SD = ±0.229) for the left eye and 0.808 (SD = ±0.310) for the right eye, suggesting normal intracranial compliance across the cohort, despite variations observed in some individuals. Physiological tests—the Valsalva maneuver and the Queckenstedt test, both performed in the supine position—induced statistically significant increases in the P2/P1 and P3/P1 ratios, supporting the notion that non-invasively recorded pressure pulse waves, measured through closed eyelids, reflect intracranial volume and pressure dynamics. Additionally, a transient hypoemic/hyperemic response test performed in the upright position induced signal changes in pressure recordings from the ‘Archimedes 02’ sensor that were consistent with intact cerebral blood flow autoregulation, aligning with established physiological principles. These findings indicate that ICP pulse waves and their dynamic changes can be monitored non-invasively through closed eyelids, offering a potential method for brain monitoring in patients for whom invasive procedures are not feasible. Full article

Radiation exposure causes neuroinflammation, oxidative stress, and neuronal loss, leading to cognitive and behavioral impairments. This study aims to evaluate the effect of niacin interventions on whole-brain irradiation (WBI)-induced cognitive and behavioral impairment. Female Wistar rats were randomly assigned to Control (Group 1), Radiation +Saline (Group 2), and Radiation +niacin (Group 3) groups. Rats in the irradiated groups (Groups 2 and 3) received a single dose of 20 Gy photon irradiation. Group 2 received water seven days after irradiation, while Group 3 received niacin (60 mg/kg, 2 mL) oral gavage for 15 days. On days 22, 23, and 24, behavioral assessments were performed, including the Open Field Test, the Sociability Test, and the Passive Avoidance Learning (PAL) task. Biochemical analyses included MDA, BDNF, TNF-α, CREB), SIRT1, and SIRT6 measured by ELISA. Histological assessments included neuronal density and GFAP immunostaining in CA1 and CA3 regions of the hippocampus and cerebellar Purkinje neurons. Radiation exposure importantly increased MDA and TNF-α levels, while SIRT1, SIRT6, BDNF, and CREB were notably reduced. This was accompanied by neuronal loss in the cerebellum and hippocampus, astrogliosis, and behavioral and cognitive deficits. Niacin treatment significantly decreased MDA and TNF-α levels while increasing BDNF, CREB, SIRT1, and SIRT6 expression, attenuating neuronal apoptosis. Immunohistochemical analysis demonstrated that niacin treatment enhanced neuronal density in the CA1 and CA3 regions of the hippocampus and cerebellar Purkinje neurons while reducing GFAP immunoreactivity in the CA1, CA3, and cerebellum following WBI. Behaviorally, niacin treatment improved social interaction, locomotor activity, and memory performance, underscoring its neuroprotective potential against WBI-induced damage. These findings suggest that niacin may ameliorate behavioral and cognitive impairments following whole brain irradiation by activating the SIRT1/CREB/BDNF or SIRT1/SIRT6/MDA/TNF-α signaling pathway. Full article

Memory impairment is a defining characteristic of Alzheimer’s disease (AD), with amnesia often appearing as its earliest symptom. Given the multifactorial nature of AD pathogenesis, this study investigates the multi-target therapeutic potential of sobrerol (coded as NRM-331) in a scopolamine-induced amnesia mouse model, focusing specifically on its effects in ameliorating memory deficits and enhancing neuronal plasticity. Sixty male C57BL/6NCrljOri mice were divided into six groups (10 mice/group): vehicle control (CTL, saline), scopolamine (SPA, 10 mg/kg/day), Aricept (APT, 2 mg/kg/day), and three treatment groups receiving NRM-331 at doses of 40, 80, and 100 mg/kg/day. Several behavioral tests were conducted, including the Y-maze test, passive avoidance test, and Morris water maze test. Additionally, biochemical assays were performed in serum (to measure Aß 1-40 and Aß 1-42) and in the brain (to assess ACh and AChE levels), along with histopathological examination of the brain using Nissl staining and p-tau IHC. No significant change was observed in the Y-maze test or the acquisition trial of the passive avoidance test. However, improvements were noted in the retention trial of the passive avoidance test and the Morris water maze test (including escape latency, swim distance, and number of platform crossed) for the NRM-331 groups compared to the SPA group. Serum levels of Aß 1-40 and Aß 1-42 decreased in the NRM-331 groups compared to the SPA group. In the brain, levels of ACh significantly increased, while AChE levels significantly decreased compared to the SPA group. The number of neuronal cells improved in the CA1, CA3, and DG regions of the hippocampus, as indicated by Nissl staining. A significant reduction in p-tau accumulation was also observed in the NRM-331 groups. In conclusion, NRM-331 demonstrated an anti-amnesic effect by enhancing hippocampal cholinergic signaling, alongside exhibiting anti-tau and anti-Aβ synthesis properties. These therapeutic effects suggest that NRM-331 significantly mitigates memory impairment induced by SPA through a neuroprotective mechanism. Full article