Traditional cardiovascular pathophysiology often relies on heart-centric models, yet the maintenance of neurocardiac homeostasis fundamentally depends on higher-order central regulation. While the bidirectional brain-heart axis is widely recognized, the spatiotemporal principles governing its network dynamics remain incompletely understood. This review presents an integrative theoretical framework to conceptualize brain-heart communication not merely as a linear reflex, but as a hierarchical, multidimensional process. We highlight the critical role of asymmetric neural regulation-where lateralized central control dictates efferent autonomic outflow-and map how this central asymmetry progressively cascades into a systemic neuro-immune-endocrine interactive network. By adopting this multiscale perspective, we delineate the mechanistic pathways through which psychological stress acts as an upstream driver to precipitate cardiovascular vulnerabilities, such as arrhythmias and heart failure. Furthermore, we discuss the translational potential of this framework, emphasizing how spatiotemporal features can be leveraged to develop dynamic biomarkers and guide precision neuromodulation therapies, ultimately providing new avenues for restoring neurocardiac homeostasis.

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the abnormal aggregation of α-synuclein (α-Syn) into Lewy bodies. While these pathological features arise from genetic susceptibility, environmental exposures, and age-related cellular deteriorations, the precise interactions among these factors remain incompletely understood. Mounting evidence implicates that copper ions are playing a critical role in PD pathogenesis, particularly in regulating dopaminergic neuron survival and the aggregation dynamics of α-Syn.

Activated HIF-1α is a key regulator of various paracrine factors that influence vascular tone, angiogenesis, and cell survival, including endothelin-1, VEGF, Ang-2, erythropoietin, and SDF-1/CXCL12. These factors not only play established roles in vascular biology but are also critical in modulating neurogenesis. The intricate relationship between the brain's vascular system and its neurogenic niches underscores the importance of HIF-1 in facilitating their interactions. Angiogenesis and proper vessel perfusion are vital for the maintenance and proliferation of neural progenitor cells, especially in the context of neurodegenerative diseases such as Alzheimer's disease (AD). In AD, impaired angiogenesis can negatively impact neurogenesis, exacerbating cognitive decline. Recent transcriptomic and proteomic studies have revealed significant upregulation of HIF-1α expression in AD patients, indicating its potential involvement in the pathophysiology of this disease. This review aims to elucidate the role of HIF-1α and related hypoxia-inducible factors in AD, focusing on their diagnostic and therapeutic implications. We specifically examine two critical neurogenic niches in the adult brain: the subventricular zone (SVZ) and the subgranular zone (SGZ). Understanding how HIF-1α affects neurogenesis in these regions may offer novel insights into potential therapeutic strategies for AD, highlighting the need for further research into the intersection of hypoxia, angiogenesis, and neurogenesis in the context of neurodegeneration. By exploring these connections, we hope to contribute to a better understanding of AD pathophysiology and identify new avenues for intervention.

Epilepsy is a neurological condition that affects around 50 million people globally. While the underlying mechanism of epilepsy is not fully understood, emerging evidence demonstrates that inflammation is a key player in the pathogenesis of epilepsy. MicroRNAs are involved in the pathogenesis of epilepsy, particularly through regulating oxidative stress, apoptosis, and inflammation. In this systematic review, we analyzed and summarized data from the literature regarding the role of inflammatory miRNAs in the pathophysiology of epilepsy, through human and animal studies. Twenty one reports on humans and 44 reports on animals were included in the current analysis. Kainic acid (KA) and pilocarpine were broadly used approaches in inducing epilepsy in animal models. Among upregulated microRNAs, miR-146a, miR-155, and miR-132 were more emphasized for their inflammatory role involved in epilepsy. MiR-221, miR-222, and miR-29a were downregulated and were associated with anti-inflammatory effects. Notably, microRNAs demonstrated tissue-specific expression patterns in different samples, including brain cortex, hippocampus, and body fluids, which is considerable in further investigations in the pathophysiologic and diagnostic roles of inflammatory microRNAs in epilepsy. Furthermore, inflammatory miRNAs regulate critical signaling pathways like TLR4/NF-κB, PI3K/Akt, and IL-1β-mediated neuroinflammation. Conclusively, these findings highlight the possibility of using inflammatory miRNAs asdiagnostic biomarkers and therapeutic targets of epilepsies.

We constructed a computational thalamocortical network model for study of the neocortical slow oscillation. It incorporated a number of neuronal types, both excitatory and inhibitory, each model neuron simulated as a multicompartment entity with numerous membrane conductances. As in previous experimental and modeling studies, simulated slow oscillations primarily depended on recurrently connected deep intrinsic bursting (IB) pyramidal cells, with NMDA receptors being critical as well as intrinsic membrane conductances (e.g. persistent Na+); and with repolarization to the Down state dependent on intrinsic (slow Ca2+-dependent K+) and synaptic (GABAB receptor mediated) conductances. Furthermore, however, we now can account for additional features of the slow oscillation: the frequent occurrence of spikelets, the presence of very fast ripple-like oscillations, and the transition to so-called fast runs (10 to ∼20 Hz bursty oscillations). These latter phenomena depended in our model on electrical coupling via gap junctions between pyramidal neurons. The importance of gap junctions is supported by previous experimental data on the ripple-blocking effect ofhalothane, as well as by data from the invitro hippocampus.

Fast spiking parvalbumin (PV) interneuron is an inhibitory gamma-aminobutyric acid (GABA)ergic interneuron diffused in different brain networks, including the cortex and hippocampus. As a key component of brain networks, PV interneurons collaborate in fundamental brain functions such as learning and memory by regulating excitation and inhibition (E/I) balance and generating gamma oscillations. The unique characteristics of PV interneurons, like their high metabolic demands and long branching axons, make them too vulnerable to stressors. Neuroinflammation is one of the most significant stressors that have an adverse, long-lasting impact on PV interneurons. Neuroinflammation affects PV interneurons through specialized inflammatory pathways triggered by cytokines such as tumor necrosis factor (TNF) and interleukin 6 (IL-6). The crucial cells in neuroinflammation, microglia, also play a significant role. The destructive effect of inflammation on PV interneurons can have comprehensive effects and cause neurological disorders such as schizophrenia, Alzheimer's disease (AD), autism spectrum disorder (ASD), and bipolar disorder. In this article, we provide a comprehensive review of mechanisms in which neuroinflammation leads to PV interneuron hypofunction in these diseases. The integrated knowledge about the role of PV interneurons in cognitive networks of the brain and mechanisms involved in PV interneuron impairment in the pathology of these diseases can help us with better therapeutic interventions.

Glioblastoma multiforme (GBM) is the most fatal brain tumor with a poor prognosis with current treatments, mainly because of intrinsic resistance processes. GBM is also referred to as grade 4 astrocytoma, that makes up about 15.4 % of brain cancers globally as well as 60-75 % of astrocytoma. The most prevalent therapeutic choices for GBM comprise surgery in combination with radiotherapy and chemotherapy, providing patients with an average survival of 6-14months. Nanocarriers provide various benefits such as enhanced drug solubility, biocompatibility, targeted activity, as well as minimized side effects. In addition, GBM treatment comes with several challenges such as the presence of the blood-brain barrier (BBB), blood-brain tumor barrier (BBTB), overexpressed efflux pumps, infiltration, invasion, drug resistance, as well as immune escape due to tumor microenvironment (TME) and cancer stem cells (CSC). Recent research has focused on nanocarriers due to their ability to self-assemble, improve bioavailability, provide controlled release, and penetrate the BBB. These nano-based components could potentially enhance drug accumulation in brain tumor tissues and reduce systemic toxicity, making them a compelling solution for GBM therapy. This review captures the complexities associated with multi-functional nano drug delivery systems (NDDS) in crossing the blood-brain barrier (BBB) and targeting cancer cells. In addition, it presents a succinct overview of various types of targeted multi-functional nano drug delivery system (NDDS) which has exhibited promising value for improving drug delivery to the brain.

Epilepsy is a group of chronic neurological brain disorders characterized by recurrent spontaneous unprovoked seizures, which are accompanied by significant neurobiological, cognitive, and psychosocial impairments. With a global prevalence of approximately 0.5-1 % of thepopulation, epilepsy remains a serious public health concern. Despite the development and widespread use of over 20 anticonvulsant drugs, around 30 % of patients continue to experience drug-resistant seizures, leading to asubstantial reduction in quality of life and increased mortality risk. Given the limited efficacy of current treatments, exploring new therapeutic approaches is critically important. In recent years, Gi-protein-coupled receptors, particularly cannabinoid receptors CB1 and CB2, have garnered increasing attention as promising targets for the treatment seizures and prevention of epilepsy. Emerging evidence suggests a significant role of the cannabinoid system in modulating neuronal activity and protecting against hyperexcitability, underscoring the importance of further research inthis area. This review provides up-to-date insights into the pathogenesis and treatment of epilepsy, with a special focus on the role of the cannabinoid system, highlighting the need for continued investigation to develop more effective therapeutic strategies.

Peripheral nerve injury (PNI) is one of the most serious causes of disability and loss of work capacity of younger individuals. Although PNS has a certain degree of regeneration, there are still challenges like disordered growth, neuroma formation, and incomplete regeneration. Regarding the management of PNI, conventional methods such as surgery, pharmacotherapy, and rehabilitative therapy. Treatment strategies vary depending on the severity of the injury. While for the long nerve defect, autologous nerve grafting is commonly recognized as the preferred surgical approach. Nevertheless, due to lack of donor sources, neurological deficits and the low regeneration efficiency of grafted nerves, nerve guide conduits (NGCs) are recognized as a future promising technology in recent years. This review provides a comprehensive overview of current treatments for PNI, and discusses NGCs from different perspectives, such as material, design, fabrication process, and composite function.