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BACKGROUND: Theta-gamma transcranial alternating current stimulation (tACS) was recently found to enhance thumb acceleration in young, healthy participants, suggesting a potential role in facilitating motor skill acquisition. Given the relevance of motor skill acquisition in stroke rehabilitation, theta-gamma tACS may hold potential for treating stroke survivors. OBJECTIVE: We aimed to examine the effects of theta-gamma tACS on motor skill acquisition in young, healthy participants and stroke survivors. METHODS: In a pre-registered, double-blind, randomized, sham-controlled study, 78 young, healthy participants received either theta-gamma peak-coupled (TGP) tACS, theta-gamma trough-coupled (TGT) tACS or sham stimulation. 20 individuals with a chronic stroke received either TGP or sham. TACS was applied over motor cortical areas while participants performed an acceleration-dependent thumb movement task. Stroke survivors were characterized using standardized testing, with a subgroup receiving additional structural brain imaging. RESULTS: Neither TGP nor TGT tACS significantly modified general motor skill acquisition in the young, healthy cohort. In contrast, in the stroke cohort, TGP diminished motor skill acquisition compared to sham. Exploratory analyses revealed that, independent of general motor skill acquisition, healthy participants receiving TGP or TGT exhibited greater peak thumb acceleration than those receiving sham. CONCLUSION: Although theta-gamma tACS increased thumb acceleration in young, healthy participants, consistent with previous reports, it did not enhance overall motor skill acquisition in a more complex motor task. Furthermore, it even had detrimental effects on motor skill acquisition in stroke survivors.

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Throughout history, various odors have been harnessed to invigorate or relax the mind. The mechanisms underlying odors' diverse arousal effects remain poorly understood. We conducted five experiments (184 participants) to investigate this issue, using pupillometry, electroencephalography, and the attentional blink paradigm, which exemplifies the limit in attentional capacity. Results demonstrated that exposure to citral, compared to vanillin, enlarged pupil size, reduced resting-state alpha oscillations and alpha network efficiency, augmented beta-gamma oscillations, and enhanced the coordination between parietal alpha and frontal beta-gamma activities. In parallel, it attenuated the attentional blink effect. These effects were observed despite citral and vanillin being comparable in perceived odor intensity, pleasantness, and nasal pungency, and were unlikely driven by semantic biases. Our findings reveal that odors differentially alter the small-worldness of brain network architecture, and thereby brain state and arousal. Furthermore, they establish arousal as a unique dimension in olfactory space, distinct from intensity and pleasantness.

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Gamma oscillations (30-120 Hz) in the brain are not periodic cycles, but they typically appear in short-time windows, often called oscillatory bursts. While the origin of this bursting phenomenon is still unclear, some recent studies hypothesize its origin in the external or endogenous noise of neural networks. We demonstrate that an exact neural mass model of excitatory and inhibitory quadratic-integrate and fire-spiking neurons theoretically predicts the emergence of a different regime of intrinsic bursting gamma (IBG) oscillations without any noise source, a phenomenon due to collective chaos. This regime is indeed observed in the direct simulation of spiking neurons, characterized by highly irregular spiking activity. IBG oscillations are distinguished by higher phase-amplitude coupling to slower theta oscillations concerning noise-induced bursting oscillations, thus indicating an increased capacity for information transfer between brain regions. We demonstrate that this phenomenon is present in both globally coupled and sparse networks of spiking neurons. These results propose a new mechanism for gamma oscillatory activity, suggesting deterministic collective chaos as a good candidate for the origin of gamma bursts.

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In order to understand how prefrontal cortex provides the benefits of working memory (WM) for visual processing we examined the influence of WM on the representation of visual signals in V4 neurons in two macaque monkeys. We found that WM induces strong ß oscillations in V4 and that the timing of action potentials relative to this oscillation reflects sensory information- i.e., a phase coding of visual information. Pharmacologically inactivating the Frontal Eye Field part of prefrontal cortex, we confirmed the necessity of prefrontal signals for the WM-driven boost in phase coding of visual information. Indeed, changes in the average firing rate of V4 neurons could be accounted for by WM-induced oscillatory changes. We present a network model to describe how WM signals can recruit sensory areas primarily by inducing oscillations within these areas and discuss the implications of these findings for a sensory recruitment theory of WM through coherence.

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Navigational decision-making tasks, such as spatial working memory (SWM), rely highly on information integration from several cortical and sub-cortical regions. Performance in SWM tasks is associated with theta rhythm, including low-frequency oscillations related to movement and memory. The interaction of the ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC), reflected in theta synchrony, is essential in various steps of information processing during SWM. We used a closed-loop neurofeedback (CLNF) system to upregulate theta power in the mPFC and investigate its effects on circuit dynamics and behavior in animal models. Specifically, we hypothesized that enhancing the power of the theta rhythm in the mPFC might improve SWM performance. Animals were divided into three groups: closed-loop (CL), random-loop (RL), and OFF (without stimulation). We recorded local field potential (LFP) in the mPFC while electrical reward stimulation contingent on cortical theta activity was delivered to the lateral hypothalamus (LH), which is considered one of the central reward-associated regions. We also recorded LFP in the vHPC to evaluate the related subcortical neural changes. Results revealed a sustained increase in the theta power in both mPFC and vHPC for the CL group. Our analysis also revealed an increase in mPFC-vHPC synchronization in the theta range over the stimulation sessions in the CL group, as measured by coherence and cross-correlation in the theta frequency band. The reinforcement of this circuit improved spatial decision-making performance in the subsequent behavioral results. Our findings provide direct evidence of the relationship between specific theta upregulation and SWM performance and suggest that theta oscillations are integral to cognitive processes. Overall, this study highlights the potential of adaptive CLNF systems in investigating neural dynamics in various brain circuits.

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Palmitoyl-protein thioesterase 1 (PPT1) is a lysosomal depalmitoylation enzyme that mediates protein posttranslational modifications. Loss-of-function mutation of PPT1 causes a failure of the lysosomal degradation of palmitoylated proteins and results in a congenital disease characterized by progressive neuronal degeneration referred to as infantile neuronal ceroid lipofuscinosis (INCL). A mouse knock-in model of PPT1 (PPT1-KI) was established by introducing the R151X mutation into exon 5 of the PPT1 gene, which exhibited INCL-like pathological lesions. We previously reported that hippocampal γ oscillations were impaired in PPT1 mice. Hippocampal γ oscillations can be enhanced by selective activation of the dopamine D4 receptor (DR4), a dopamine D2-like receptor. In this study, we investigated the changes in DR expression and the effects of dopamine and various DR agonists on neural network activity, cognition and motor function in PPT1KI mice. Cognition and motor defects were evaluated via Y-maze, novel object recognition and rotarod tests. Extracellular field potentials were elicited in hippocampal slices, and neuronal network oscillations in the gamma frequency band (γ oscillations) were induced by perfusion with kainic acid (200 nM). PPT1KI mice displayed progressive impairments in γ oscillations and hippocampus-related memory, as well as abnormal expression profiles of dopamine receptors with preserved expression of DR1 and 3, increased membrane expression of DR4 and decreased DR2 levels. The immunocytochemistry analysis revealed the colocalization of PPT1 with DR4 or DR2 in the soma and large dendrites of both WT and PPT1KI mice. Immunoprecipitation confirmed the interaction between PPT1 and DR4 or DR2. The impaired γ oscillations and cognitive functions were largely restored by the application of exogenous dopamine, the selective DR2 agonist quinpirole or the DR4 agonist A412997. Furthermore, the administration of A412997 (0.5 mg/kg, i.p.) significantly upregulated the activity of CaMKII in the hippocampus of 5-month-old PPT1KI mice. Collectively, these results suggest that the activation of D2-like dopamine receptors improves cognition and network activity in PPT1KI mice and that specific DR subunits may be potential targets for the intervention of neurodegenerative disorders, such as INCL.

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As of now, all over the world is focusing on the Electric Vehicle (EV) technology because its features are low environmental pollution, less maitainence cost required, high robustness, and good dynamic response. Also, the EVs work continuously until the input fuel is provided to the fuel stack. Here, a Proton Exchange Membrane Fuel Cell (PEMFC) is used as an input source to the electric vehicle system because of its merits fast startup, and quick response. However, the PEMFC gives nonlinear voltage versus current characteristics. As a result, the extraction of maximum power from the fuel stack is very difficult. The main aim of this work is to study different Maximum Power Point Tracking Techniques (MPPT) for the DC-DC converter-fed PEMFC system. The studied MPPT controllers are Adjusted Step Value of Perturb & Observe (ASV with P&O), Adaptive Step Size with Incremental Conductance (ASS with IC), Radial Basis Functional Network (RBFN), Incremental Step-Fuzzy Logic Controller (IS with FLC), Continuous Step Variation based Particle Swarm Optimization (CSV with PSO), and Adaptive Step Value-Cuckoo Search Algorithm (ASV with CSA). The selected MPPT controllers' comprehensive study has been in terms of maximum power extraction, tracking speed of the MPP, settling time of the fuel stack output voltage, oscillations across the MPP, and design complexity. From the comprehensive performance results of the hybrid MPPT controllers, the ASV with CSA technique gives superior performance when equated to the other MPPT controllers.

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The quest for intrinsically ferromagnetic topological materials is a focal point in the study of topological phases of matter, as intrinsic ferromagnetism plays a vital role in realizing exotic properties such as the anomalous Hall effect (AHE) in quasi-two-dimensional materials, and this stands out as one of the most pressing concerns within the field. Here, we investigate a novel higher order member of the MnSb2nTe3n+1family, MnSb12Te19, for the first time combining magnetotransport and angle-resolved photoemission spectroscopy (ARPES) measurements. Our magnetic susceptibility experiments identify ferromagnetic transitions at temperatureTc= 18.7 K, consistent with our heat capacity measurements (T= 18.8 K). The AHE is observed for the field along thec-axis belowTc. Our study of Shubinikov-de-Haas oscillations provides evidence for Dirac fermions withπBerry phase. Our comprehensive investigation reveals that MnSb12Te19exhibits a FM ground state along with AHE, and hole-dominated transport properties consistent with ARPES measurements.

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Schizophrenia is believed to be, at least in part, a dysfunction of the glutamatergic system. In line with anatomical evidence, suppressing N-methyl-D-aspartate (NMDA) neurotransmission leads to symptoms that are characteristic of schizophrenia. Rodent models of schizophrenia often involve the acute application of NMDA antagonists, which produce both behavioural and brain activity changes that closely resemble symptoms observed in schizophrenia. It is, however, important to note that the full spectrum of schizophrenia symptoms may not be manifested following the acute suppression of NMDA receptors. This has led to the proposal of a chronic model where NMDA receptors are suppressed for prolonged periods. Although the chronic model has shown promising results from a behavioural perspective and alterations in metabolic processes in the brain, its impact on brain oscillations remains largely unknown. The aim of this study is to examine the impact of acute and chronic NMDA neurotransmission suppression on brains' oscillatory activity. To achieve this, chronic brain activity recordings in mice of both sexes were used to assess both spontaneous and evoked brain oscillations. The study demonstrates that an acute suppression of NMDA receptors alters brain oscillations across a wide frequency spectrum and diminishes the oscillatory potency in evoked responses, paralleling changes observed in schizophrenia. However, the chronic suppression of NMDA receptors did not have the expected cumulative effect on brain activity. This research highlights the robust yet similar impacts of acute and chronic NMDA receptor suppression on brain activity, contributing to the nuanced understanding of rodent models of schizophrenia.

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The electrical activity of the brain, characterized by its frequency components, reflects a complex interplay between periodic (oscillatory) and aperiodic components. These components are associated with various neurophysiological processes, such as the excitation-inhibition balance (aperiodic activity) or interregional communication (oscillatory activity). However, we do not fully understand whether these components are truly independent or if different neuromodulators modulate them in different ways. The dopaminergic system has a critical role for cognition and motivation, being a potential modulator of these power spectrum components. To improve our understanding of these questions, we investigated the differential effects of this system on these components using electrocorticogram recordings in cats, which show clear oscillations and aperiodic 1/f activity. Specifically, we focused on the effects of haloperidol (a D2 receptor antagonist) on oscillatory and aperiodic dynamics during wakefulness and sleep. By parameterizing the power spectrum into these two components, our findings reveal a state-dependent modulation of oscillatory activity by the D2 receptor across the brain. Surprisingly, aperiodic activity was not significantly affected and exhibited inconsistent changes across the brain. This suggests a nuanced interplay between neuromodulation and the distinct components of brain oscillations, providing insights into the selective regulation of oscillatory dynamics in awake states.

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Oscillatory complex networks in the metastable regime have been used to study the emergence of integrated and segregated activity in the brain, which are hypothesised to be fundamental for cognition. Yet, the parameters and the underlying mechanisms necessary to achieve the metastable regime are hard to identify, often relying on maximising the correlation with empirical functional connectivity dynamics. Here, we propose and show that the brain's hierarchically modular mesoscale structure alone can give rise to robust metastable dynamics and (metastable) chimera states in the presence of phase frustration. We construct unweighted 3-layer hierarchical networks of identical Kuramoto-Sakaguchi oscillators, parameterized by the average degree of the network and a structural parameter determining the ratio of connections between and within blocks in the upper two layers. Together, these parameters affect the characteristic timescales of the system. Away from the critical synchronization point, we detect the emergence of metastable states in the lowest hierarchical layer coexisting with chimera and metastable states in the upper layers. Using the Laplacian renormalization group flow approach, we uncover two distinct pathways towards achieving the metastable regimes detected in these distinct layers. In the upper layers, we show how the symmetry-breaking states depend on the slow eigenmodes of the system. In the lowest layer instead, metastable dynamics can be achieved as the separation of timescales between layers reaches a critical threshold. Our results show an explicit relationship between metastability, chimera states, and the eigenmodes of the system, bridging the gap between harmonic based studies of empirical data and oscillatory models.

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Near-death experience (NDE) is a transcendent mental event of uncertain etiology that arises on the cusp of biological death. Since the discovery of NDE in the mid-1970s, multiple neuroscientific theories have been developed in an attempt to account for it in strictly materialistic or reductionistic terms. Therefore, in this conception, NDE is at most an extraordinary hallucination without any otherworldly, spiritual, or supernatural denotations. During the last decade or so, a number of animal and clinical studies have emerged which reported that about the time of death, there may be a surge of high frequency electroencephalogram (EEG) at a time when cortical electrical activity is otherwise at a very low ebb. This oscillatory rhythm falls within the range of the enigmatic brain wave-labelled gamma-band activity (GBA). Therefore, it has been proposed that this brief, paradoxical, and perimortem burst of the GBA may represent the neural foundation of the NDE. This study examines three separate but related questions concerning this phenomenon. The first problem pertains to the electrogenesis of standard GBA and the extent to which authentic cerebral activity has been contaminated by myogenic artifacts. The second problem involves the question of whether agents that can mimic NDE are also underlain by GBA. The third question concerns the electrogenesis of the surge in GBA itself. It has been contended that this is neither cortical nor myogenic in origin. Rather, it arises in a subcortical (amygdaloid) location but is recorded at the cortex via volume conduction, thereby mimicking standard GBA. Although this surge of GBA contains genuine electrophysiological activity and is an intriguing and provocative finding, there is little evidence to suggest that it could act as a kind of neurobiological skeleton for a phenomenon such as NDE.

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Calcium (Ca2+) is a second messenger for many signal pathways, and changes in intracellular Ca2+ concentration ([Ca2+]i) are an important signaling mechanism in the oocyte maturation, activation, fertilization, function regulation of granulosa and cumulus cells and offspring development. Ca2+ oscillations occur during oocyte maturation and fertilization, which are maintained by Ca2+ stores and extracellular Ca2+ ([Ca2+]e). Abnormalities in Ca2+ signaling can affect the release of the first polar body, the first meiotic division, and chromosome and spindle morphology. Well-studied aspects of Ca2+ signaling in the oocyte are oocyte activation and fertilization. Oocyte activation, driven by sperm-specific phospholipase PLCζ, is initiated by concerted intracellular patterns of Ca2+ release, termed Ca2+ oscillations. Ca2+ oscillations persist for a long time during fertilization and are coordinately engaged by a variety of Ca2+ channels, pumps, regulatory proteins and their partners. Calcium signaling also regulates granulosa and cumulus cells' function, which further affects oocyte maturation and fertilization outcome. Clinically, there are several physical and chemical options for treating fertilization failure through oocyte activation. Additionally, various exogenous compounds or drugs can cause ovarian dysfunction and female infertility by inducing abnormal Ca2+ signaling or Ca2+ dyshomeostasis in oocytes and granulosa cells. Therefore, the reproductive health risks caused by adverse stresses should arouse our attention. This review will systematically summarize the latest research progress on the aforementioned aspects and propose further research directions on calcium signaling in female reproduction.

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The cell division cycle is a fundamental physiological process displaying a great degree of plasticity during the course of multicellular development. This plasticity is evident in the transition from rapid and stringently-timed divisions of the early embryo to subsequent size-controlled mitotic cycles. Later in development, cells may pause and restart proliferation in response to myriads of internal or external signals, or permanently exit the cell cycle following terminal differentiation or senescence. Beyond this, cells can undergo modified cell division variants, such as endoreplication, which increases their ploidy, or meiosis, which reduces their ploidy. This wealth of behaviours has led to numerous conceptual analogies intended as frameworks for understanding the proliferative program. Here, we aim to unify these mechanisms under one dynamical paradigm. To this end, we take a control theoretical approach to frame the cell cycle as a pair of arrestable and mutually-inhibiting, doubly amplified, negative feedback oscillators controlling chromosome replication and segregation events, respectively. Under appropriate conditions, this framework can reproduce fixed-period oscillations, checkpoint arrests of variable duration, and endocycles. Subsequently, we use phase plane and bifurcation analysis to explain the dynamical basis of these properties. Then, using a physiologically realistic, biochemical model, we show that the very same regulatory structure underpins the diverse functions of the cell cycle control network. We conclude that Newton's cradle may be a suitable mechanical analogy of how the cell cycle is regulated.

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OBJECTIVES: Healthy age-related cognitive changes are highly heterogeneous across individuals. This variability is increasingly explained through the lens of spontaneous fluctuations of brain activity, now considered as powerful index of age-related changes. However, brain activity is a biological process modulated by circadian rhythms, and how these fluctuations evolve throughout the day is under investigated. METHODS: We analyzed data from one hundred and one healthy late middle-aged participants from the Cognitive Fitness in Aging study (68 women and 33 men; aged 50-69 years). Participants completed five EEG recordings of spontaneous resting-state activity on the same day. We used weighted phase-lag index (wPLI) analyses as an index of the functional synchrony between brain regions couplings and we computed daily global PLI fluctuation rates of the five recordings to assess the association with cognitive performance and ß-amyloid and tau/neuroinflammation pathological markers. RESULTS: We found that theta and gamma daily fluctuations in the salience-control executive inter-network (SN-CEN) are associated with distinct mechanisms underlying cognitive heterogeneity in aging. Higher levels of SN-CEN theta daily fluctuations appear to be deleterious for memory performance and were associated with higher tau/neuroinflammation rates. In contrast, higher levels of gamma daily fluctuations are positively associated with executive performance, and were associated with lower rate of ß-amyloid deposition. DISCUSSION: Thus, accounting for daily EEG fluctuations of brain activity contributes to better understand subtle brain changes underlying individuals' cognitive performance in healthy aging. Results also provide arguments for considering time-of-day when assessing cognition for old adults in a clinical context.

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This proposed model explores the intricate Ca2+ dynamics within the pancreatic acinar cells (PACs) by emphasizing the role of store-operated Ca2+ entry (SOCE) and the mitochondrial-associated membranes (MAMs) in the secretory region (apical) of the PACs. Traditionally, Ca2+ releases from the endoplasmic reticulum (ER) via calcium-induced calcium release (CICR). It has been shown to be important in regulating functions such as secretion of digestive enzymes in PACs. However, this model posits that upon the depletion of Ca2+ in the ER, the signaling protein stromal interaction molecule (STIM1) is activated. Activated STIM1, then facilitates the opening of Orai channels, allowing Ca2+ influx through the store-operated calcium channels (SOCCs). The model highlights the complexity of the Ca2+ dynamics, and the importance of SOCE and MAMs in the PACs Ca2+ homeostasis. The numerical and bifurcation analysis illustrate how changes in agonist concentrations can lead to the diverse Ca2+ oscillation patterns, such as thin to broader oscillations, sinusoidal patterns, and baseline fluctuations, driven by the feedback mechanisms involving Ca2+ and inositol 1,4,5 trisphosphate (IP3). This understanding could have broader implications for cellular physiology and the development of therapies targeting Ca2+ signaling pathways.

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It has been found that the intraday dynamics of body temperature in small mammal and bird species on the adjacent day are similar. Therefore, by focusing on the body temperature dynamics of the previous day, it is possible to predict with a high degree of accuracy the periods of increase and decrease in body temperature for the current day. This phenomenon was observed when animals were kept under natural illumination and under artificial illumination when the phase of the intrinsic circadian rhythm shifted by 1-2 h every day. When analyzing this phenomenon in birds, it has been shown that the best match for body temperature dynamics occurs when comparing adjacent days based on sidereal days (a period of 23 h and 56 min). Over time, after several days, the daily patterns of body temperature fluctuation take on a completely different form and frequency. These facts suggest a connection between ultradian rhythms and the rotation of the Earth around its axis, and consequently, the position of animals on the surface of the planet relative to space objects.

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Cell replacement therapies using medial ganglionic eminence (MGE)-derived GABAergic precursors reduce seizures by restoring inhibition in animal models of epilepsy. However, how MGE-derived cells affect abnormal neuronal networks and consequently brain oscillations to reduce ictogenesis is still under investigation. We performed quantitative analysis of pre-ictal local field potentials (LFP) of cortical and hippocampal CA1 areas recorded in vivo in the pilocarpine rat model of epilepsy, with or without intrahippocampal MGE-precursor grafts (PILO and PILO+MGE groups, respectively). The PILO+MGE animals had a significant reduction in the number of seizures. The quantitative analysis of pre-ictal LFP showed decreased power of cortical and hippocampal delta, theta and beta oscillations from the 5 min. interictal baseline to the 20 s. pre-ictal period in both groups. However, PILO+MGE animals had higher power of slow and fast oscillations in the cortex and lower power of slow and fast oscillations in the hippocampus compared to the PILO group. Additionally, PILO+MGE animals exhibited decreased cortico-hippocampal synchrony for theta and gamma oscillations at seizure onset and lower hippocampal CA1 synchrony between delta and theta with slow gamma oscillations compared to PILO animals. These findings suggest that MGE-derived cell integration into the abnormally rewired network may help control ictogenesis.

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Much of our understanding of how the brain processes dynamic faces comes from research that compares static photographs to dynamic morphs, which exhibit simplified, computer-generated motion. By comparing static, video recorded, and dynamic morphed expressions, we aim to identify the neural correlates of naturalistic facial dynamism, using time-domain and time-frequency analysis. Dynamic morphs were made from the neutral and peak frames of video recorded transitions of happy and fearful expressions, which retained expression change and removed asynchronous and non-linear features of naturalistic facial motion. We found that dynamic morphs elicited increased N400 amplitudes and lower LPP amplitudes compared to other stimulus types. Video recordings elicited higher LPP amplitudes and greater frontal delta activity compared to other stimuli. Thematic analysis of participant interviews using a large language model revealed that participants found it difficult to assess the genuineness of morphed expressions, and easier to analyse the genuineness of happy compared to fearful expressions. Our findings suggest that animating real faces with artificial motion may violate expectations (N400) and reduce the social salience (LPP) of dynamic morphs. Results also suggest that delta oscillations in the frontal region may be involved with the perception of naturalistic facial motion in happy and fearful expressions. Overall, our findings highlight the sensitivity of neural mechanisms required for face perception to subtle changes in facial motion characteristics, which has important implications for neuroimaging research using faces with simplified motion.

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Background: Parkinson's disease (PD) is a prevalent neurodegenerative disorder affecting millions globally. It encompasses both motor and non-motor symptoms, with a notable impact on patients' quality of life. Electroencephalogram (EEG) is a non-invasive tool that is increasingly utilized to investigate neural mechanisms in PD, identify early diagnostic markers, and assess therapeutic responses. Methods: The data were sourced from the Science Citation Index Expanded within the Web of Science Core Collection database, focusing on publications related to EEG research in PD from 2004 to 2023. A comprehensive bibliometric analysis was conducted using CiteSpace and VOSviewer software. The analysis began with an evaluation of the selected publications, identifying leading countries, institutions, authors, and journals, as well as co-cited references, to summarize the current state of EEG research in PD. Keywords are employed to identify research topics that are currently of interest in this field through the analysis of high-frequency keyword co-occurrence and cluster analysis. Finally, burst keywords were identified to uncover emerging trends and research frontiers in the field, highlighting shifts in interest and identifying future research directions. Results: A total of 1,559 publications on EEG research in PD were identified. The United States, Germany, and England have made notable contributions to the field. The University of London is the leading institution in terms of publication output, with the University of California closely following. The most prolific authors are Brown P, Fuhr P, and Stam C In terms of total citations and per-article citations, Stam C has the highest number of citations, while Brown P has the highest H-index. In terms of the total number of publications, Clinical Neurophysiology is the leading journal, while Brain is the most highly cited. The most frequently cited articles pertain to software toolboxes for EEG analysis, neural oscillations, and PD pathophysiology. Through analyzing the keywords, four research hotspots were identified: research on the neural oscillations and connectivity, research on the innovations in EEG Analysis, impact of therapies on EEG, and research on cognitive and emotional assessments. Conclusion: This bibliometric analysis demonstrates a growing global interest in EEG research in PD. The investigation of neural oscillations and connectivity remains a primary focus of research. The application of machine learning, deep learning, and task analysis techniques offers promising avenues for future research in EEG and PD, suggesting the potential for advancements in this field. This study offers valuable insights into the major research trends, influential contributors, and evolving themes in this field, providing a roadmap for future exploration.