Introduction:

University students are frequently exposed to high cognitive demands, which can lead to sustained cognitive load and mental fatigue and may negatively affect learning outcomes and well-being. Electroencephalography (EEG) provides a non-invasive, real-time window into neural activity associated with cognitive effort. This systematic review aims to synthesise current evidence on EEG markers of cognitive load and mental fatigue in university students and other young adult learners.

Methods:

This systematic review was conducted in accordance with the PRISMA 2020 statement (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). We systematically searched electronic databases (e.g., PubMed, Scopus and Web of Science) for peer-reviewed studies on EEG-based assessment of cognitive load/mental fatigue in healthy young adults (typically university students). Records were screened against predefined inclusion/exclusion criteria, and eligible studies were included for data extraction.

Results:

Seven studies met the inclusion criteria, comprising 179 participants (sample sizes 7–43). Paradigms varied across examination stress, language-mediated learning, multimedia manipulations, and classroom tasks, limiting direct comparisons. Cognitive load was most often reflected in changes in theta, alpha, and beta power and band ratios. One study found that self-reported difficulty correlated positively with beta activity at T3 (r = 0.309, p < 0.05) and negatively with learning performance (r = −0.391, p < 0.01). Studies manipulating multimedia design principles generally reported lower load indicators and better test performance when principles were applied.

Conclusions:

EEG-based markers, particularly theta and posterior alpha activity, show promising potential for indexing cognitive load and mental fatigue in university students. However, methodological variability and small sample sizes hinder the development of robust, generalisable EEG metrics. Future research should prioritise standardised protocols, larger cohorts and transparent reporting to support the use of EEG for monitoring cognitive strain in educational and applied settings.

Introduction. The mammalian spinal cord consists of myelinated axons forming the white matter (WM) and neurons forming the gray matter (GM). The ratio of WM to GM areas (WM/GM) is a well-known macroanatomical characteristic of the spinal cord. This ratio is lower within cervical and lumbar enlargements and higher between them (in the thoracic region). It also varies significantly across species: for example, in the upper lumbar segments, it is lower in rats but higher in horses. We hypothesized that this species-dependent variation might be (at least partially) explained by the degree of spinal cord ascension.

Methods. We assessed the level of SC ascension and WM/GM ratio of the spinal cord segments in the African hedgehog. Based on the literature data from other mammals (goat, European hedgehog, horse, human, mouse, opossum, pig, rabbit, rat, rhesus macaque, and mole), we performed phylogenetic correlations between the WM/GM ratio of the L1–L5 lumbar segments and the level of ascension, defined as the number of the vertebra where the 29th spinal cord segment was located.

Results. We found that in African hedgehog, similarly to European hedgehog, the spinal cord is highly ascended, and the WM/GM ratio in all lumbar segments is less than those in other mammalian species. The phylogenetic correlation was significant for all lumbar segments studied (L1 and L5: p < 0.05; L2–L4: p < 0.01).

Conclusion. The WM/GM ratio of the lumbar spinal cord segments is significantly correlated with the degree of spinal cord ascension: the higher the ascension, the lower the WM/GM ratio. This relationship may be explained by the fact that a longer spinal cord requires a relatively larger volume of conducting pathways to exchange the same amount of information with the brain.

Cognitive decline in AD extends beyond global memory impairment, encompassing deficits in working memory, cognitive flexibility, recognition processes, and the integration of exploratory strategies. Dissecting these components in transgenic models offers an opportunity to refine our understanding of how distinct neurobiological perturbations shape cognitive architecture under neurodegenerative conditions.

This study presents a comparative cognitive analysis of six hexanic fractions derived from Rubus fruticosus in the 5xFAD mouse model of AD. Transgenic mice were assigned to treatment groups receiving individual fractions at two concentrations (50mg/kg and 100mg/kg; n=10 per fraction) alongside control groups (NaCl,n=5; galantamine, n=5). All treatments were administered orally for seven consecutive days, one hour prior to behavioral assessment.

Cognitive performance was evaluated using a battery of tasks designed to probe complementary domains of cognition: spontaneous alternation (Y-Maze), recognition memory and encoding efficiency (Novel Object Recognition), and working and reference memory organization (Radial Arm Maze). Additional measures of exploratory behavior and emotional modulation were obtained using the Open Field, Elevated Plus Maze, and the Forced Swimming Test to contextualize cognitive outcomes within broader behavioral states. In silico pharmacokinetic and target-prediction analyses were conducted to support interpretation of behavioral variability across fractions.

Comparative behavioral profiling revealed fraction-specific cognitive signatures, indicating that distinct fractions differentially modulate cognitive subdomains rather than producing uniform enhancements across tasks. Several fractions exhibited non-linear dose–response relationships, with lower doses preferentially influencing memory accuracy and task-specific strategies, while higher doses primarily affected locomotor or exploratory parameters. These dissociations suggest that cognitive outcomes in the 5xFAD model reflect complex interactions between fraction-specific phytochemical composition and disease-related alterations in neural circuitry.

This study underscores the value of comparative cognitive phenotyping in transgenic models of AD. Integrating in silico predictions with multidimensional behavioral analysis provides a framework for interpreting divergent cognitive effects across chemically related fractions.

The heart, brain, and gastrointestinal tract have long been examined as separate electrophysiological domains, each with its own clinical tools and diagnostic language. However, emerging evidence points to a deeper, bioelectrically coordinated relationship among these systems—one that has remained largely unexplored in both research and practice. This work introduces the Tri-Electrical Axis (TEA), a novel physiological framework proposing that the cardiac, cerebral, and enteric systems form a synchronized regulatory network governed by shared electrical patterns. Rather than treating ECG, EEG, and electroenterographic (EEnG) signals as isolated modalities, TEA emphasizes their dynamic interactions and latent harmonies. Initial analyses of co-registered cardiac and cerebral signals reveal reproducible phase coupling and feedback loops suggestive of an integrated bioelectrical substrate. These findings support the hypothesis that multi-organ synchrony may play a role in homeostasis, adaptive responses, and even early disease manifestation. The upcoming inclusion of enteric electrophysiology is expected to complete this triadic structure, offering a richer model of systemic physiology. More than a methodological innovation, TEA represents a conceptual shift: it challenges organ-specific silos and reimagines human physiology as an interdependent, signal-driven system. Such a model holds transformative potential for preventive medicine, enabling earlier detection of dysfunctions that manifest first in cross-organ desynchronization rather than isolated pathology. By uncovering this hidden electrical axis, the TEA framework offers a foundation for future diagnostics, dynamic monitoring tools, and integrative research across cardiology, neurology, and gastroenterology. It is not only a new way to analyze signals—but a new way to understand life.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has had a profound and lasting impact on global public health. Beyond the acute phase of infection, many people develop Long COVID-19, a condition characterized by the persistence or appearance of new symptoms weeks or months after recovery. Among the most common and debilitating symptoms are olfactory and gustatory disorders, which significantly impair quality of life weeks or months after recovery.

This study aimed to investigate the frequency and characteristics of self-reported symptoms across three distinct phases—pre-infection, acute COVID-19, and post-acute (Long COVID-19)—focusing on chemosensory disturbances and cognitive abilities. To this end, an anonymous online questionnaire was administered, incorporating validated instruments and specific questions regarding participants’ clinical history. In addition, a subgroup of participants residing in Sardinia (Italy), specifically in the Cagliari area, underwent objective assessments of olfactory and gustatory functions using standardized tests integrating subjective reports with clinical experimental measures.

The results revealed a marked reduction in systemic symptoms from the acute to the post-acute phase; however, olfactory and gustatory impairments persisted in a substantial proportion of individuals, particularly among women and participants under 25 years of age. Our data show a significant correlation between chemosensory deficits and cognitive impairments. In conclusion, the results indicate that chemosensory dysfunction may serve as a potential clinical biomarker of Long COVID-19 and highlight the need for longitudinal studies to clarify the underlying pathophysiological mechanisms and guide the development of targeted therapeutic interventions.

Background: Autism Spectrum Disorder is a complex neurodevelopmental condition with a strong genetic basis, yet the molecular mechanisms by which many risk-associated variants disrupt neuronal function remain poorly understood. CSDE1, a post-transcriptional regulator implicated in neurodevelopment, has recently emerged as a candidate susceptibility gene in Autism Spectrum Disorder, although the structural and functional consequences of its coding variants remain largely unexplored.

Objective: This study aimed to systematically characterize the structural and dynamic effects of nonsynonymous single-nucleotide polymorphisms in CSDE1 associated with Autism Spectrum Disorder using an integrative computational framework.

Methods: A comprehensive in silico pipeline was employed to prioritize potentially deleterious CSDE1 variants using sequence- and structure-based prediction tools, including SIFT, PolyPhen-2, MutPred2, I-Mutant 2.0, MUpro, DynaMut, and ConSurf. The CSDE1 protein structure was obtained from the AlphaFold Protein Structure Database, refined using GalaxyRefine, and validated with MolProbity. Functionally relevant domains harboring high-confidence variants were subjected to all-atom molecular dynamics simulations. Structural dynamics were evaluated over 100 ns simulation trajectories using root mean square deviation, root mean square fluctuation, radius of gyration, hydrogen bond occupancy, and solvent-accessible surface area.

Results: Comparative analyses between wild-type and mutant CSDE1 proteins revealed pronounced conformational instability, altered residue flexibility, disrupted compactness, and changes in intramolecular interaction networks in selected variants. These perturbations suggest compromised structural integrity and functional dynamics of CSDE1, supporting their potential pathogenic relevance in Autism Spectrum Disorder.

Conclusion:This study provides the first detailed molecular-level characterization of Autism Spectrum Disorder-associated CSDE1 nonsynonymous variants using computational modeling and molecular dynamics simulations. The findings highlight candidate variants with functional relevance and establish a framework for future experimental validation, offering insights into the mechanistic role of CSDE1 in neurodevelopmental dysfunction and its potential utility as a molecular biomarker.

Hearing loss profoundly affects individuals’ quality of life, limiting participation in social, professional, and communicative domains. Cochlear implants (CIs) restore access to auditory input for postlingually deafened adults, but understanding speech through a CI relies heavily on neuroplastic adaptation. While many CI users regain the ability to follow conversations in quiet environments, speech-in-noise (SPiN) perception remains a major challenge. Music training has been shown to enhance shared auditory and cognitive neural networks and to improve auditory-motor coupling, which may facilitate SPiN perception in both normal-hearing and hearing-impaired individuals. These findings provide a rationale for using multi-modal Neurologic Music Therapy (NMT™) to support auditory rehabilitation in adult CI users. However, research to date has focused primarily on passive music listening, leaving the effects of structured, active music training largely unexplored. This randomized controlled clinical trial investigates the effects of short-term targeted multi-modal music training on SPiN and working memory (WM) in postlingually deafened adult CI users. Additionally, the study examines neurophysiological mechanisms of change using electroencephalography (EEG), specifically focusing on alpha oscillation modulations during auditory-cognitive tasks. Thirty-six adult CI users are enrolled in a 4-week NMT™ training program, randomly assigned to pitch, rhythm, or timbre-focused conditions. Behavioral outcomes are assessed pre- and post-training using the sentence-final-word-identification-and-recall (SWIR) test; EEG is recorded during all SWIR tasks. Presented will be behavioral results from 36 participants on SPiN perception and WM performance between training types. So far, only behavioral data have been analyzed; EEG analysis is ongoing and will be reported as available. Early findings, based on a small and heterogeneous sample, show promising trends. Further EEG analysis is expected to provide deeper insight into neuroplastic changes, including modulation of alpha activity, potentially supporting music-based strategies to enhance auditory performance and life quality in CI users.

Introduction: Alzheimer’s disease (AD) is characterized by progressive cognitive decline and is largely driven by amyloid-β aggregation, tau hyperphosphorylation and widespread synaptic dysfunction. Chronic neuroinflammation, associated with altered cytokine signalling, plays a significant role in the progression of AD. Although nicotine has been shown to influence inflammatory pathways, its therapeutic use is constrained by adverse effects. 6-hydroxy-L-nicotine (6HLN), a nicotine metabolite, may exhibit anti-inflammatory activity while offering a more favorable safety profile. In this context, the present study examines the effects of 6HLN on specific molecular markers of inflammatory cytokine signalling to assess its potential biological relevance in AD-associated pathology.

Methods: The effects of chronic 6HLN treatment were evaluated in a 5xFAD transgenic mouse model of AD. 5xFAD mice underwent chronic intraperitoneal administration of 6HLN at two doses (0.3 and 0.6mg/kg for 30 days). Key inflammatory mediators (NF-κB, IL-6 and TNF-α) were quantified from brain homogenates using ELISA.

Results: 6HLN induced a dose-dependent reduction in NF-κB, IL-6 and TNF-α levels, indicating a significant attenuation of pro-inflammatory cytokine response in 5xFAD mice.

Conclusion: These findings suggest that 6HLN may serve as a promising anti-inflammatory candidate for mitigating inflammation-related pathological processes in AD. This work was supported by CNCSIS-UEFISCSU, project number PN-III-P4-PCE-2021-1692.

The amygdala is an important part of the human brain that helps control individual feelings. It is connected to emotions, fear, and memory, and works closely with other areas of the brain. Techniques like transcranial electrical stimulation, which includes direct current stimulation, and transcranial alternating of the current stimulation change how the human brain works and influence behavior when electrical currents are applied. Most of the information about these electrical fields comes from computer models. Surprisingly, there have only been a few studies on the human brain that looked at the effects of directly stimulating the amygdala. This includes how it affects human emotional and physical reactions. Cognitive sciences still do not fully understand the exact emotional and physical changes that occur with this form of stimulation. Understanding how stimulating the amygdala impacts emotions is imperative for contemporary ideas about how feelings work in the human brain. These ideas present different viewpoints on the effect of stimulation on emotions. Studies that use functional neuroimaging proffer concrete substantiation for the significant function of the amygdala in handling emotions. To explore these discussions, this paper offers systematic review methods incorporating a structured literature search to document the entire process, ensure reproducibility, and minimize bias. This was conducted to examine functional neuroimaging research that examines how the human brain reacts to emotional representations that activate the amygdala. Our analysis specifically considered both the strength of the effects and the consistency of each activation, unlike past studies. Findings in this study suggest that the amygdala reacts to both positive and depressing emotionsthat demonstrate feelings. In conclusion, the results from this structured literature search and systematic review paper provide new insights into various theories and models discussed in contemporary research about how the human brain processes emotions.

Background: The management of advanced Parkinson's disease (PD) is often complicated by the failure of conventional oral therapies to provide sustained symptom control. PD patients progressively develop debilitating motor fluctuations and "OFF" periods, alongside long-term treatment complications which severely impact functional autonomy. Advanced PD is also characterized by a heavy burden of non-motor symptoms (NMS), including neuropsychiatric features, sleep disturbances, and autonomic dysfunction. These NMS are often underestimated but profoundly impact overall well-being. Strategic management of these patients can be improved by the administration of infusion therapies which represent a critical advancement in addressing these challenges. In this scenario, continuous delivery of levodopa-carbidopa intestinal gel (enteral), subcutaneous foslevodopa/foscarbidopa and apomorphine (subcutaneous) may be useful to achieve a more stable and continuous pharmacokinetic profile compared to pulsatile oral dosing. Strategic administration of infusion therapies represents a major advancement in addressing these challenges.

Objective: To describe the primary impact of this strategy in the significant reduction not only on motor fluctuations but also on non-motor fluctuations.

Discussion: PD infusion therapies are related to the concept of continuous dopaminergic stimulation and dramatically are able not only to reduce motor "OFF" time and duration of dyskinesias but also to significantly improve non-motor fluctuations, restoring functional independence and enhancing patients' quality of life. In fact, the efficacy of infusion therapy extends beyond motor control. Its strategic management is fundamentally reliant on a comprehensive, multidisciplinary care model. This team-based approach allows for intensive monitoring during dose titration and long-term follow-up, enabling the active identification and treatment of NMS.

Conclusions: Tailored infusion PD treatments represent a cornerstone of advanced PD care. Its success is optimized when embedded within a strategic, multidisciplinary framework that utilizes advanced monitoring to concurrently manage both motor and non-motor symptoms, leading to superior clinical outcomes.