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15 January 2026, Volume 21 Issue 1 Previous Issue   

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Exosomes in stroke management: A promising paradigm shift in stroke therapy Bo Wang, Pinzhen Chen, Wenyan Li, Zhi Chen 2026, 21 (1):  6-22.  doi: 10.4103/NRR.NRR-D-24-00665 Abstract ( 79 )   PDF (6947KB) ( 46 )   Save Effective treatment methods for stroke, a common cerebrovascular disease with a high mortality rate, are still being sought. Exosome therapy, a form of acellular therapy, has demonstrated promising efficacy in various diseases in animal models; however, there is currently insufficient evidence to guide the clinical application of exosome in patients with stroke. This article reviews the progress of exosome applications in stroke treatment. It aims to elucidate the significant potential value of exosomes in stroke therapy and provide a reference for their clinical translation. At present, many studies on exosome-based therapies for stroke are actively underway. Regarding preclinical research, exosomes, as bioactive substances with diverse sources, currently favor stem cells as their origin. Due to their high plasticity, exosomes can be effectively modified through various physical, chemical, and genetic engineering methods to enhance their efficacy. In animal models of stroke, exosome therapy can reduce neuroinflammatory responses, alleviate oxidative stress damage, and inhibit programmed cell death. Additionally, exosomes can promote angiogenesis, repair and regenerate damaged white matter fiber bundles, and facilitate the migration and differentiation of neural stem cells, aiding the repair process. We also summarize new directions for the application of exosomes, specifically the exosome intervention through the ventricular–meningeal lymphatic system. The review findings suggest that the treatment paradigm for stroke is poised for transformation. Related Articles | Metrics

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Epilepsy therapy beyond neurons: Unveiling astrocytes as cellular targets Yuncan Chen, Jiayi Hu, Ying Zhang, Lulu Peng, Xiaoyu Li, Cong Li, Xunyi Wu, Cong Wang 2026, 21 (1):  23-38.  doi: 10.4103/NRR.NRR-D-24-01035 Abstract ( 63 )   PDF (11913KB) ( 23 )   Save Epilepsy is a leading cause of disability and mortality worldwide. However, despite the availability of more than 20 antiseizure medications, more than one-third of patients continue to experience seizures. Given the urgent need to explore new treatment strategies for epilepsy, recent research has highlighted the potential of targeting gliosis, metabolic disturbances, and neural circuit abnormalities as therapeutic strategies. Astrocytes, the largest group of nonneuronal cells in the central nervous system, play several crucial roles in maintaining ionic and energy metabolic homeostasis in neurons, regulating neurotransmitter levels, and modulating synaptic plasticity. This article briefly reviews the critical role of astrocytes in maintaining balance within the central nervous system. Building on previous research, we discuss how astrocyte dysfunction contributes to the onset and progression of epilepsy through four key aspects: the imbalance between excitatory and inhibitory neuronal signaling, dysregulation of metabolic homeostasis in the neuronal microenvironment, neuroinflammation, and the formation of abnormal neural circuits. We summarize relevant basic research conducted over the past 5 years that has focused on modulating astrocytes as a therapeutic approach for epilepsy. We categorize the therapeutic targets proposed by these studies into four areas: restoration of the excitation–inhibition balance, reestablishment of metabolic homeostasis, modulation of immune and inflammatory responses, and reconstruction of abnormal neural circuits. These targets correspond to the pathophysiological mechanisms by which astrocytes contribute to epilepsy. Additionally, we need to consider the potential challenges and limitations of translating these identified therapeutic targets into clinical treatments. These limitations arise from interspecies differences between humans and animal models, as well as the complex comorbidities associated with epilepsy in humans. We also highlight valuable future research directions worth exploring in the treatment of epilepsy and the regulation of astrocytes, such as gene therapy and imaging strategies. The findings presented in this review may help open new therapeutic avenues for patients with drugresistant epilepsy and for those suffering from other central nervous system disorders associated with astrocytic dysfunction. Related Articles | Metrics

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Microglial polarization pathways and therapeutic drugs targeting activated microglia in traumatic brain injury Liping Shi, Shuyi Liu, Jialing Chen, Hong Wang, Zhengbo Wang 2026, 21 (1):  39-56.  doi: 10.4103/NRR.NRR-D-24-00810 Abstract ( 55 )   PDF (3699KB) ( 72 )   Save Traumatic brain injury can be categorized into primary and secondary injuries. Secondary injuries are the main cause of disability following traumatic brain injury, which involves a complex multicellular cascade. Microglia play an important role in secondary injury and can be activated in response to traumatic brain injury. In this article, we review the origin and classification of microglia as well as the dynamic changes of microglia in traumatic brain injury. We also clarify the microglial polarization pathways and the therapeutic drugs targeting activated microglia. We found that regulating the signaling pathways involved in pro-inflammatory and anti-inflammatory microglia, such as the Toll-like receptor 4 /nuclear factor-kappa B, mitogen-activated protein kinase, Janus kinase/signal transducer and activator of transcription, phosphoinositide 3-kinase/protein kinase B, Notch, and high mobility group box 1 pathways, can alleviate the inflammatory response triggered by microglia in traumatic brain injury, thereby exerting neuroprotective effects. We also reviewed the strategies developed on the basis of these pathways, such as drug and cell replacement therapies. Drugs that modulate inflammatory factors, such as rosuvastatin, have been shown to promote the polarization of antiinflammatory microglia and reduce the inflammatory response caused by traumatic brain injury. Mesenchymal stem cells possess anti-inflammatory properties, and clinical studies have confirmed their significant efficacy and safety in patients with traumatic brain injury. Additionally, advancements in mesenchymal stem cell-delivery methods—such as combinations of novel biomaterials, genetic engineering, and mesenchymal stem cell exosome therapy—have greatly enhanced the efficiency and therapeutic effects of mesenchymal stem cells in animal models. However, numerous challenges in the application of drug and mesenchymal stem cell treatment strategies remain to be addressed. In the future, new technologies, such as single-cell RNA sequencing and transcriptome analysis, can facilitate further experimental studies. Moreover, research involving non-human primates can help translate these treatment strategies to clinical practice. Related Articles | Metrics

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Hidden face of Parkinson’s disease: Is it a new autoimmune disease? Min Gi Jo, Seon-Hee Kim, Seung Pil Yun 2026, 21 (1):  57-61.  doi: 10.4103/NRR.NRR-D-24-01063 Abstract ( 39 )   PDF (3807KB) ( 45 )   Save Parkinson’s disease is a neurodegenerative disorder marked by the degeneration of dopaminergic neurons and clinical symptoms such as tremors, rigidity, and slowed movements. A key feature of Parkinson’s disease is the accumulation of misfolded α-synuclein, forming insoluble Lewy bodies in the substantia nigra pars compacta, which contributes to neurodegeneration. These α-synuclein aggregates may act as autoantigens, leading to T-cell-mediated neuroinflammation and contributing to dopaminergic cell death. Our perspective explores the hypothesis that Parkinson’s disease may have an autoimmune component, highlighting research that connects peripheral immune responses with neurodegeneration. T cells derived from Parkinson’s disease patients appear to have the potential to initiate an autoimmune response against α-synuclein and its modified peptides, possibly leading to the formation of neo-epitopes. Recent evidence associates Parkinson’s disease with abnormal immune responses, as indicated by increased levels of immune cells, such as CD4+ and CD8+ T cells, observed in both patients and mouse models. The convergence of T cells filtration increasing major histocompatibility complex molecules, and the susceptibility of dopaminergic neurons supports the hypothesis that Parkinson’s disease may exhibit autoimmune characteristics. Understanding the immune mechanisms involved in Parkinson’s disease will be crucial for developing therapeutic strategies that target the autoimmune aspects of the disease. Novel approaches, including precision medicine based on major histocompatibility complex/human leukocyte antigen typing and early biomarker identification, could pave the way for immune-based treatments aimed at slowing or halting disease progression. This perspective explores the relationship between autoimmunity and Parkinson’s disease, suggesting that further research could deepen understanding and offer new therapeutic avenues. In this paper, it is organized to provide a comprehensive perspective on the autoimmune aspects of Parkinson’s disease. It investigates critical areas such as the autoimmune response observed in Parkinson’s disease patients and the role of autoimmune mechanisms targeting α-synuclein in Parkinson’s disease. The paper also examines the impact of CD4+ T cells, specifically Th1 and Th17, on neurons through in vitro and ex vivo studies. Additionally, it explores how α-synuclein influences glia-induced neuroinflammation in Parkinson’s disease. The discussion extends to the clinical implications and therapeutic landscape, offering insights into potential treatments. Consequently, we aim to provide a comprehensive perspective on the autoimmune aspects of Parkinson’s disease, incorporating both supportive and opposing views on its classification as an autoimmune disorder and exploring implications for clinical applications. Related Articles | Metrics

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NLRP3 inflammasome and gut microbiota–brain axis: A new perspective on white matter injury after intracerebral hemorrhage Xiaoxi Cai, Xinhong Cai, Quanhua Xie, Xueqi Xiao, Tong Li, Tian Zhou, Haitao Sun 2026, 21 (1):  62-80.  doi: 10.4103/NRR.NRR-D-24-00917 Abstract ( 51 )   PDF (7400KB) ( 18 )   Save Intracerebral hemorrhage is the most dangerous subtype of stroke, characterized by high mortality and morbidity rates, and frequently leads to significant secondary white matter injury. In recent decades, studies have revealed that gut microbiota can communicate bidirectionally with the brain through the gut microbiota–brain axis. This axis indicates that gut microbiota is closely related to the development and prognosis of intracerebral hemorrhage and its associated secondary white matter injury. The NACHT, LRR, and pyrin domain-containing protein 3 (NLRP3) inflammasome plays a crucial role in this context. This review summarizes the dysbiosis of gut microbiota following intracerebral hemorrhage and explores the mechanisms by which this imbalance may promote the activation of the NLRP3 inflammasome. These mechanisms include metabolic pathways (involving short-chain fatty acids, lipopolysaccharides, lactic acid, bile acids, trimethylamine-N-oxide, and tryptophan), neural pathways (such as the vagus nerve and sympathetic nerve), and immune pathways (involving microglia and T cells). We then discuss the relationship between the activated NLRP3 inflammasome and secondary white matter injury after intracerebral hemorrhage. The activation of the NLRP3 inflammasome can exacerbate secondary white matter injury by disrupting the blood–brain barrier, inducing neuroinflammation, and interfering with nerve regeneration. Finally, we outline potential treatment strategies for intracerebral hemorrhage and its secondary white matter injury. Our review highlights the critical role of the gut microbiota–brain axis and the NLRP3 inflammasome in white matter injury following intracerebral hemorrhage, paving the way for exploring potential therapeutic approaches. Related Articles | Metrics

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Dual effects of GABAAR agonist anesthetics in neurodevelopment and vulnerable brains: From neurotoxic to therapeutic effects Dihan Lu, Wen Zhang, Keyu Chen, Xia Feng 2026, 21 (1):  81-95.  doi: 10.4103/NRR.NRR-D-24-00828 Abstract ( 38 )   PDF (2945KB) ( 36 )   Save Debates regarding the specific effects of general anesthesia on developing brains have persisted for over 30 years. A consensus has been reached that prolonged, repeated, high-dose exposure to anesthetics is associated with a higher incidence of deficits in behavior and executive function, while single exposure has a relatively minor effect on long-term neurological function. In this review, we summarize the dose-dependent neuroprotective or neurotoxic effects of gamma-aminobutyric acid type A receptor agonists, a representative group of sedatives, on developing brains or central nervous system diseases. Most preclinical research indicates that anesthetics have neurotoxic effects on the developing brain through various signal pathways. However, recent studies on low-dose anesthetics suggest that they may promote neurodevelopment during this critical period. These findings are incomprehensible for the general “dose-effect” principles of pharmacological research, which has attracted researchers’ interest and led to the following questions: What is the threshold for the dual effects exerted by anesthetics such as propofol and sevoflurane on the developing brain? To what extent can their protective effects be maximized? What are the underlying mechanisms involved in these effects? Consequently, this issue has essentially become a “mathematical problem.” After summarizing the dose-dependent effects of gamma-aminobutyric acid type A receptor agonist sedatives in both the developing brain and the brains of patients with central nervous system diseases, we believe that all such anesthetics exhibit specific threshold effects unique to each drug. These effects range from neuroprotection to neurotoxicity, depending on different brain functional states. However, the exact values of the specific thresholds for different drugs in various brain states, as well as the underlying mechanisms explaining why these thresholds exist, remain unclear. Further in-depth exploration of these issues could significantly enhance the therapeutic translational value of these anesthetics. Related Articles | Metrics

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Adiponectin as a potential mediator of the pro-cognitive effects of physical exercise on Alzheimer’s disease Hui-Hui Guo, Hai-Ning Ou, Jia-Sui Yu, Julia Macedo Rosa, Douglas Affonso Formolo, Tong Cheng, Suk-Yu Yau, Hector Wing Hong Tsang 2026, 21 (1):  96-106.  doi: 10.4103/NRR.NRR-D-23-00943 Abstract ( 23 )   PDF (4475KB) ( 35 )   Save Alzheimer’s disease is the primary cause of dementia and imposes a significant socioeconomic burden globally. Physical exercise, as an effective strategy for improving general health, has been largely reported for its effectiveness in slowing neurodegeneration and increasing brain functional plasticity, particularly in aging brains. However, the underlying mechanisms of exercise in cognitive aging remain largely unclear. Adiponectin, a cell-secreted protein hormone, has recently been found to regulate synaptic plasticity and mediate the antidepressant effects of physical exercise. Studies on the neuroprotective effects of adiponectin have revealed potential innovative treatments for Alzheimer’s disease. Here, we reviewed the functions of adiponectin and its receptor in the brains of human and animal models of cognitive impairment. We summarized the role of adiponectin in Alzheimer’s disease, focusing on its impact on energy metabolism, insulin resistance, and inflammation. We also discuss how exercise increases adiponectin secretion and its potential benefits for learning and memory. Finally, we highlight the latest research on chemical compounds that mimic exerciseenhanced secretion of adiponectin and its receptor in Alzheimer’s disease. Related Articles | Metrics

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Neuronal plasticity and its role in Alzheimer’s disease and Parkinson’s disease Israt Jahan, Mohammad Harun-Ur-Rashid, Md. Aminul Islam, Farhana Sharmin, Soad K. Al Jaouni, Abdullah M. Kaki, Samy Selim 2026, 21 (1):  107-125.  doi: 10.4103/NRR.NRR-D-24-01019 Abstract ( 90 )   PDF (2768KB) ( 49 )   Save Neuronal plasticity, the brain’s ability to adapt structurally and functionally, is essential for learning, memory, and recovery from injuries. In neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, this plasticity is disrupted, leading to cognitive and motor deficits. This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer’s disease and Parkinson’s disease. Alzheimer’s disease features amyloid-beta plaques and tau tangles that impair synaptic function, while Parkinson’s disease involves the loss of dopaminergic neurons affecting motor control. Enhancing neuronal plasticity offers therapeutic potential for these diseases. A systematic literature review was conducted using databases such as PubMed, Scopus, and Google Scholar, focusing on studies of neuronal plasticity in Alzheimer’s disease and Parkinson’s disease. Data synthesis identified key themes such as synaptic mechanisms, neurogenesis, and therapeutic strategies, linking molecular insights to clinical applications. Results highlight that targeting synaptic plasticity mechanisms, such as long-term potentiation and long-term depression, shows promise. Neurotrophic factors, advanced imaging techniques, and molecular tools (e.g., clustered regularly interspaced short palindromic repeats and optogenetics) are crucial in understanding and enhancing plasticity. Current therapies, including dopamine replacement, deep brain stimulation, and lifestyle interventions, demonstrate the potential to alleviate symptoms and improve outcomes. In conclusion, enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases. Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer’s disease and Parkinson’s disease. Related Articles | Metrics

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Emerging role of microglia in the developing dopaminergic system: Perturbation by early life stress Kaijie She, Naijun Yuan, Minyi Huang, Wenjun Zhu, Manshi Tang, Qingyu Ma, Jiaxu Chen 2026, 21 (1):  126-140.  doi: 10.4103/NRR.NRR-D-24-00742 Abstract ( 67 )   PDF (6711KB) ( 14 )   Save Early life stress correlates with a higher prevalence of neurological disorders, including autism, attention-deficit/hyperactivity disorder, schizophrenia, depression, and Parkinson’s disease. These conditions, primarily involving abnormal development and damage of the dopaminergic system, pose significant public health challenges. Microglia, as the primary immune cells in the brain, are crucial in regulating neuronal circuit development and survival. From the embryonic stage to adulthood, microglia exhibit stage-specific gene expression profiles, transcriptome characteristics, and functional phenotypes, enhancing the susceptibility to early life stress. However, the role of microglia in mediating dopaminergic system disorders under early life stress conditions remains poorly understood. This review presents an up-to-date overview of preclinical studies elucidating the impact of early life stress on microglia, leading to dopaminergic system disorders, along with the underlying mechanisms and therapeutic potential for neurodegenerative and neurodevelopmental conditions. Impaired microglial activity damages dopaminergic neurons by diminishing neurotrophic support (e.g., insulin-like growth factor-1) and hinders dopaminergic axon growth through defective phagocytosis and synaptic pruning. Furthermore, blunted microglial immunoreactivity suppresses striatal dopaminergic circuit development and reduces neuronal transmission. Furthermore, inflammation and oxidative stress induced by activated microglia can directly damage dopaminergic neurons, inhibiting dopamine synthesis, reuptake, and receptor activity. Enhanced microglial phagocytosis inhibits dopamine axon extension. These long-lasting effects of microglial perturbations may be driven by early life stress–induced epigenetic reprogramming of microglia. Indirectly, early life stress may influence microglial function through various pathways, such as astrocytic activation, the hypothalamic–pituitary–adrenal axis, the gut–brain axis, and maternal immune signaling. Finally, various therapeutic strategies and molecular mechanisms for targeting microglia to restore the dopaminergic system were summarized and discussed. These strategies include classical antidepressants and antipsychotics, antibiotics and anti-inflammatory agents, and herbal-derived medicine. Further investigations combining pharmacological interventions and genetic strategies are essential to elucidate the causal role of microglial phenotypic and functional perturbations in the dopaminergic system disrupted by early life stress. Related Articles | Metrics

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Current understanding and prospects for targeting neurogenesis in the treatment of cognitive impairment Ye Liu, Xibing Ding, Shushan Jia, Xiyao Gu 2026, 21 (1):  141-155.  doi: 10.4103/NRR.NRR-D-24-00802 Abstract ( 47 )   PDF (2932KB) ( 52 )   Save Adult hippocampal neurogenesis is linked to memory formation in the adult brain, with new neurons in the hippocampus exhibiting greater plasticity during their immature stages compared to mature neurons. Abnormal adult hippocampal neurogenesis is closely associated with cognitive impairment in central nervous system diseases. Targeting and regulating adult hippocampal neurogenesis have been shown to improve cognitive deficits. This review aims to expand the current understanding and prospects of targeting neurogenesis in the treatment of cognitive impairment. Recent research indicates the presence of abnormalities in AHN in several diseases associated with cognitive impairment, including cerebrovascular diseases, Alzheimer’s disease, aging-related conditions, and issues related to anesthesia and surgery. The role of these abnormalities in the cognitive deficits caused by these diseases has been widely recognized, and targeting AHN is considered a promising approach for treating cognitive impairment. However, the underlying mechanisms of this role are not yet fully understood, and the effectiveness of targeting abnormal adult hippocampal neurogenesis for treatment remains limited, with a need for further development of treatment methods and detection techniques. By reviewing recent studies, we classify the potential mechanisms of adult hippocampal neurogenesis abnormalities into four categories: immunity, energy metabolism, aging, and pathological states. In immunity-related mechanisms, abnormalities in meningeal, brain, and peripheral immunity can disrupt normal adult hippocampal neurogenesis. Lipid metabolism and mitochondrial function disorders are significant energy metabolism factors that lead to abnormal adult hippocampal neurogenesis. During aging, the inflammatory state of the neurogenic niche and the expression of aging-related microRNAs contribute to reduced adult hippocampal neurogenesis and cognitive impairment in older adult patients. Pathological states of the body and emotional disorders may also result in abnormal adult hippocampal neurogenesis. Among the current strategies used to enhance this form of neurogenesis, physical therapies such as exercise, transcutaneous electrical nerve stimulation, and enriched environments have proven effective. Dietary interventions, including energy intake restriction and nutrient optimization, have shown efficacy in both basic research and clinical trials. However, drug treatments, such as antidepressants and stem cell therapy, are primarily reported in basic research, with limited clinical application. The relationship between abnormal adult hippocampal neurogenesis and cognitive impairment has garnered widespread attention, and targeting the former may be an important strategy for treating the latter. However, the mechanisms underlying abnormal adult hippocampal neurogenesis remain unclear, and treatments are lacking. This highlights the need for greater focus on translating research findings into clinical practice. Related Articles | Metrics

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Cerebellar microglia: On the edge between neuroinflammation and neuroregulation Marina S. Dukhinova, Jingwen Guo, Enwei Shen, Wanting Liu, Wanqi Huang, Ying Shen, Luxi Wang 2026, 21 (1):  156-172.  doi: 10.4103/NRR.NRR-D-24-00550 Abstract ( 53 )   PDF (4215KB) ( 74 )   Save The cerebellum is receiving increasing attention for its cognitive, emotional, and social functions, as well as its unique metabolic profiles. Cerebellar microglia exhibit specialized and highly immunogenic phenotypes under both physiological and pathological conditions. These immune cells communicate with intrinsic and systemic factors and contribute to the structural and functional compartmentalization of the cerebellum. In this review, we discuss the roles of microglia in the cerebellar microenvironment, neuroinflammation, cerebellar adaptation, and neuronal activity, the associated molecular and cellular mechanisms, and potential therapeutic strategies targeting cerebellar microglia in the context of neuroinflammation. Future directions and unresolved questions in this field are further highlighted, particularly regarding therapeutic interventions targeting cerebellar microglia, functional mechanisms and activities of microglia in the cerebellar circuitry, neuronal connectivity, and neurofunctional outcomes of their activity. Cerebellar morphology and neuronal performance are influenced by both intrinsic and systemic factors that are actively monitored by microglia in both healthy and diseased states. Under pathological conditions, local subsets of microglia exhibit diverse responses to the altered microenvironment that contribute to the structural and functional compartmentalization of the cerebellum. Microglia in the cerebellum undergo early maturation during the embryonic stage and display specialized, highly immunogenic phenotypes. In summary, cerebellar microglia have the capacity to serve as regulatory tools that influence outcomes across a wide range of neurological and systemic conditions, including neurodevelopmental, neurodegenerative, metabolic, and stress-related disorders. Related Articles | Metrics

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Neural functional rehabilitation: Exploring neuromuscular reconstruction technology advancements and challenges Chunxiao Tang, Ping Wang, Zhonghua Li, Shizhen Zhong, Lin Yang, Guanglin Li 2026, 21 (1):  173-186.  doi: 10.4103/NRR.NRR-D-24-00613 Abstract ( 60 )   PDF (14903KB) ( 10 )   Save Neural machine interface technology is a pioneering approach that aims to address the complex challenges of neurological dysfunctions and disabilities resulting from conditions such as congenital disorders, traumatic injuries, and neurological diseases. Neural machine interface technology establishes direct connections with the brain or peripheral nervous system to restore impaired motor, sensory, and cognitive functions, significantly improving patients’ quality of life. This review analyzes the chronological development and integration of various neural machine interface technologies, including regenerative peripheral nerve interfaces, targeted muscle and sensory reinnervation, agonist–antagonist myoneural interfaces, and brain–machine interfaces. Recent advancements in flexible electronics and bioengineering have led to the development of more biocompatible and highresolution electrodes, which enhance the performance and longevity of neural machine interface technology. However, significant challenges remain, such as signal interference, fibrous tissue encapsulation, and the need for precise anatomical localization and reconstruction. The integration of advanced signal processing algorithms, particularly those utilizing artificial intelligence and machine learning, has the potential to improve the accuracy and reliability of neural signal interpretation, which will make neural machine interface technologies more intuitive and effective. These technologies have broad, impactful clinical applications, ranging from motor restoration and sensory feedback in prosthetics to neurological disorder treatment and neurorehabilitation. This review suggests that multidisciplinary collaboration will play a critical role in advancing neural machine interface technologies by combining insights from biomedical engineering, clinical surgery, and neuroengineering to develop more sophisticated and reliable interfaces. By addressing existing limitations and exploring new technological frontiers, neural machine interface technologies have the potential to revolutionize neuroprosthetics and neurorehabilitation, promising enhanced mobility, independence, and quality of life for individuals with neurological impairments. By leveraging detailed anatomical knowledge and integrating cutting-edge neuroengineering principles, researchers and clinicians can push the boundaries of what is possible and create increasingly sophisticated and long-lasting prosthetic devices that provide sustained benefits for users. Related Articles | Metrics

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GEMIN5 and neurodevelopmental diseases: From functional insights to disease perception Encarnacion Martinez-Salas , Rosario Francisco-Velilla 2026, 21 (1):  187-194.  doi: 10.4103/NRR.NRR-D-24-01010 Abstract ( 30 )   PDF (1001KB) ( 51 )   Save GEMIN5 is a predominantly cytoplasmic multifunctional protein, known to be involved in recognizing snRNAs through its WD40 repeats domain placed at the N-terminus. A dimerization domain in the middle region acts as a hub for protein–protein interaction, while a non-canonical RNA-binding site is placed towards the C-terminus. The singular organization of structural domains present in GEMIN5 enables this protein to perform multiple functions through its ability to interact with distinct partners, both RNAs and proteins. This protein exerts a different role in translation regulation depending on its physiological state, such that while GEMIN5 down-regulates global RNA translation, the C-terminal half of the protein promotes translation of its mRNA. Additionally, GEMIN5 is responsible for the preferential partitioning of mRNAs into polysomes. Besides selective translation, GEMIN5 forms part of distinct ribonucleoprotein complexes, reflecting the dynamic organization of macromolecular complexes in response to internal and external signals. In accordance with its contribution to fundamental cellular processes, recent reports described clinical loss of function mutants suggesting that GEMIN5 deficiency is detrimental to cell growth and survival. Remarkably, patients carrying GEMIN5 biallelic variants suffer from neurodevelopmental delay, hypotonia, and cerebellar ataxia. Molecular analyses of individual variants, which are defective in protein dimerization, display decreased levels of ribosome association, reinforcing the involvement of the protein in translation regulation. Importantly, the number of clinical variants and the phenotypic spectrum associated with GEMIN5 disorders is increasing as the knowledge of the protein functions and the pathways linked to its activity augments. Here we discuss relevant advances concerning the functional and structural features of GEMIN5 and its separate domains in RNA-binding, protein interactome, and translation regulation, and how these data can help to understand the involvement of protein malfunction in clinical variants found in patients developing neurodevelopmental disorders. Related Articles | Metrics

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Investigation of epilepsy-related genes in a Drosophila model Xiaochong Qu, Xiaodan Lai, Mingfeng He, Jinyuan Zhang, Binbin Xiang, Chuqiao Liu, Ruina Huang, Yiwu Shi, Jingda Qiao 2026, 21 (1):  195-211.  doi: 10.4103/NRR.NRR-D-24-00877 Abstract ( 35 )   PDF (6858KB) ( 86 )   Save Complex genetic architecture is the major cause of heterogeneity in epilepsy, which poses challenges for accurate diagnosis and precise treatment. A large number of epilepsy candidate genes have been identified from clinical studies, particularly with the widespread use of next-generation sequencing. Validating these candidate genes is emerging as a valuable yet challenging task. Drosophila serves as an ideal animal model for validating candidate genes associated with neurogenetic disorders such as epilepsy, due to its rapid reproduction rate, powerful genetic tools, and efficient use of ethological and electrophysiological assays. Here, we systematically summarize the advantageous techniques of the Drosophila model used to investigate epilepsy genes, including genetic tools for manipulating target gene expression, ethological assays for seizure-like behaviors, electrophysiological techniques, and functional imaging for recording neural activity. We then introduce several typical strategies for identifying epilepsy genes and provide new insights into gene‒gene interactions in epilepsy with polygenic causes. We summarize well-established precision medicine strategies for epilepsy and discuss prospective treatment options, including drug therapy and gene therapy for genetic epilepsy based on the Drosophila model. Finally, we also address genetic counseling and assisted reproductive technology as potential approaches for the prevention of genetic epilepsy. Related Articles | Metrics

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Enhanced neurogenesis after ischemic stroke: The interplay between endogenous and exogenous stem cells Ruxu Geng, Yuhe Wang, Renzhi Wang, Jun Wu, Xinjie Bao 2026, 21 (1):  212-223.  doi: 10.4103/NRR.NRR-D-24-00879 Abstract ( 46 )   PDF (2340KB) ( 29 )   Save Ischemic stroke is a significant global health crisis, frequently resulting in disability or death, with limited therapeutic interventions available. Although various intrinsic reparative processes are initiated within the ischemic brain, these mechanisms are often insufficient to restore neuronal functionality. This has led to intensive investigation into the use of exogenous stem cells as a potential therapeutic option. This comprehensive review outlines the ontogeny and mechanisms of activation of endogenous neural stem cells within the adult brain following ischemic events, with focus on the impact of stem cell-based therapies on neural stem cells. Exogenous stem cells have been shown to enhance the proliferation of endogenous neural stem cells via direct cell-tocell contact and through the secretion of growth factors and exosomes. Additionally, implanted stem cells may recruit host stem cells from their niches to the infarct area by establishing so-called “biobridges.” Furthermore, xenogeneic and allogeneic stem cells can modify the microenvironment of the infarcted brain tissue through immunomodulatory and angiogenic effects, thereby supporting endogenous neuroregeneration. Given the convergence of regulatory pathways between exogenous and endogenous stem cells and the necessity for a supportive microenvironment, we discuss three strategies to simultaneously enhance the therapeutic efficacy of both cell types. These approaches include: (1) co-administration of various growth factors and pharmacological agents alongside stem cell transplantation to reduce stem cell apoptosis; (2) synergistic administration of stem cells and their exosomes to amplify paracrine effects; and (3) integration of stem cells within hydrogels, which provide a protective scaffold for the implanted cells while facilitating the regeneration of neural tissue and the reconstitution of neural circuits. This comprehensive review highlights the interactions and shared regulatory mechanisms between endogenous neural stem cells and exogenously implanted stem cells and may offer new insights for improving the efficacy of stem cell-based therapies in the treatment of ischemic stroke. Related Articles | Metrics

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Adeno-associated viral vectors for modeling Parkinson’s disease in non-human primates Julia Chocarro, José L. Lanciego 2026, 21 (1):  224-232.  doi: 10.4103/NRR.NRR-D-24-00896 Abstract ( 29 )   PDF (14044KB) ( 3 )   Save The development of clinical candidates that modify the natural progression of sporadic Parkinson’s disease and related synucleinopathies is a praiseworthy endeavor, but extremely challenging. Therapeutic candidates that were successful in preclinical Parkinson’s disease animal models have repeatedly failed when tested in clinical trials. While these failures have many possible explanations, it is perhaps time to recognize that the problem lies with the animal models rather than the putative candidate. In other words, the lack of adequate animal models of Parkinson’s disease currently represents the main barrier to preclinical identification of potential disease-modifying therapies likely to succeed in clinical trials. However, this barrier may be overcome by the recent introduction of novel generations of viral vectors coding for different forms of alpha-synuclein species and related genes. Although still facing several limitations, these models have managed to mimic the known neuropathological hallmarks of Parkinson’s disease with unprecedented accuracy, delineating a more optimistic scenario for the near future. Related Articles | Metrics

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Targeting the glymphatic system to promote α-synuclein clearance: a novel therapeutic strategy for Parkinson’s disease Xiaoyue Lian, Zhenghao Liu, Zuobin Gan, Qingshan Yan, Luyao Tong, Linan Qiu, Yuntao Liu, Jiang-fan Chen, Zhihui Li 2026, 21 (1):  233-247.  doi: 10.4103/NRR.NRR-D-24-00764 Abstract ( 41 )   PDF (3250KB) ( 96 )   Save The excessive buildup of neurotoxic α-synuclein plays a pivotal role in the pathogenesis of Parkinson’s disease, highlighting the urgent need for innovative therapeutic strategies to promote α-synuclein clearance, particularly given the current lack of disease-modifying treatments. The glymphatic system, a recently identified perivascular fluid transport network, is crucial for clearing neurotoxic proteins. This review aims to synthesize current knowledge on the role of the glymphatic system in α-synuclein clearance and its implications for the pathology of Parkinson’s disease while emphasizing potential therapeutic strategies and areas for future research. The review begins with an overview of the glymphatic system and details its anatomical structure and physiological functions that facilitate cerebrospinal fluid circulation and waste clearance. It summarizes emerging evidence from neuroimaging and experimental studies that highlight the close correlation between the glymphatic system and clinical symptom severity in patients with Parkinson’s disease, as well as the effect of glymphatic dysfunction on α-synuclein accumulation in Parkinson’s disease models. Subsequently, the review summarizes the mechanisms of glymphatic system impairment in Parkinson’s disease, including sleep disturbances, aquaporin-4 impairment, and mitochondrial dysfunction, all of which diminish glymphatic system efficiency. This creates a vicious cycle that exacerbates α-synuclein accumulation and worsens Parkinson’s disease. The therapeutic perspectives section outlines strategies for enhancing glymphatic activity, such as improving sleep quality and pharmacologically targeting aquaporin-4 or its subcellular localization. Promising interventions include deep brain stimulation, melatonin supplementation, γ-aminobutyric acid modulation, and non-invasive methods (such as exercise and bright-light therapy), multisensory γ stimulation, and ultrasound therapy. Moreover, identifying neuroimaging biomarkers to assess glymphatic flow as an indicator of α-synuclein burden could refine Parkinson’s disease diagnosis and track disease progression. In conclusion, the review highlights the critical role of the glymphatic system in α-synuclein clearance and its potential as a therapeutic target in Parkinson’s disease. It advocates for further research to elucidate the specific mechanisms by which the glymphatic system clears misfolded α-synuclein and the development of imaging biomarkers to monitor glymphatic activity in patients with Parkinson’s disease. Findings from this review suggest that enhancing glymphatic clearance is a promising strategy for reducing α-synuclein deposits and mitigating the progression of Parkinson’s disease. Related Articles | Metrics

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Synaptic and synchronic impairments in subcortical brain regions associated with early non-cognitive dysfunction in Alzheimer’s disease Nicolás Riffo-Lepe, Juliana González-Sanmiguel, Lorena Armijo-Weingart, Paulina Saavedra-Sieyes, David Hernandez, Gerson Ramos, Loreto S. San Martín, Luis G. Aguayo 2026, 21 (1):  248-264.  doi: 10.4103/NRR.NRR-D-24-01052 Abstract ( 35 )   PDF (13716KB) ( 6 )   Save For many decades, Alzheimer’s disease research has primarily focused on impairments within cortical and hippocampal regions, which are thought to be related to cognitive dysfunctions such as memory and language deficits. The exact cause of Alzheimer’s disease is still under debate, making it challenging to establish an effective therapy or early diagnosis. It is widely accepted that the accumulation of amyloid-beta peptide in the brain parenchyma leads to synaptic dysfunction, a critical step in Alzheimer’s disease development. The traditional amyloid cascade model is initiated by accumulating extracellular amyloid-beta in brain areas essential for memory and language. However, while it is possible to reduce the presence of amyloid-beta plaques in the brain with newer immunotherapies, cognitive symptoms do not necessarily improve. Interestingly, recent studies support the notion that early alterations in subcortical brain regions also contribute to brain damage and precognitive decline in Alzheimer’s disease. A body of recent evidence suggests that early Alzheimer’s disease is associated with alterations (e.g., motivation, anxiety, and motor impairment) in subcortical areas, such as the striatum and amygdala, in both human and animal models. Also, recent data indicate that intracellular amyloid-beta appears early in subcortical regions such as the nucleus accumbens, locus coeruleus, and raphe nucleus, even without extracellular amyloid plaques. The reported effects are mainly excitatory, increasing glutamatergic transmission and neuronal excitability. In agreement, data in Alzheimer’s disease patients and animal models show an increase in neuronal synchronization that leads to electroencephalogram disturbances and epilepsy. The data indicate that early subcortical brain dysfunctions might be associated with non-cognitive symptoms such as anxiety, irritability, and motivation deficits, which precede memory loss and language alterations. Overall, the evidence reviewed suggests that subcortical brain regions could explain early dysfunctions and perhaps be targets for therapies to slow disease progression. Future research should focus on these non-traditional brain regions to reveal early pathological alterations and underlying mechanisms to advance our understanding of Alzheimer’s disease beyond the traditionally studied hippocampal and cortical circuits. Related Articles | Metrics

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Potential mechanisms of non-coding RNA regulation in Alzheimer’s disease Yue Sun, Xinping Pang, Xudong Huang, Dinglu Liu, Jingyue Huang, Pengtao Zheng, Yanyu Wei, Chaoyang Pang 2026, 21 (1):  265-280.  doi: 10.4103/NRR.NRR-D-24-00696 Abstract ( 35 )   PDF (8473KB) ( 2 )   Save Alzheimer’s disease, a progressively degenerative neurological disorder, is the most common cause of dementia in the elderly. While its precise etiology remains unclear, researchers have identified diverse pathological characteristics and molecular pathways associated with its progression. Advances in scientific research have increasingly highlighted the crucial role of non-coding RNAs in the progression of Alzheimer’s disease. These non-coding RNAs regulate several biological processes critical to the advancement of the disease, offering promising potential as therapeutic targets and diagnostic biomarkers. Therefore, this review aims to investigate the underlying mechanisms of Alzheimer’s disease onset, with a particular focus on microRNAs, long non-coding RNAs, and circular RNAs associated with the disease. The review elucidates the potential pathogenic processes of Alzheimer’s disease and provides a detailed description of the synthesis mechanisms of the three aforementioned non-coding RNAs. It comprehensively summarizes the various non-coding RNAs that have been identified to play key regulatory roles in Alzheimer’s disease, as well as how these noncoding RNAs influence the disease’s progression by regulating gene expression and protein functions. For example, miR-9 targets the UBE4B gene, promoting autophagy-mediated degradation of Tau protein, thereby reducing Tau accumulation and delaying Alzheimer’s disease progression. Conversely, the long non-coding RNA BACE1-AS stabilizes BACE1 mRNA, promoting the generation of amyloid-β and accelerating Alzheimer’s disease development. Additionally, circular RNAs play significant roles in regulating neuroinflammatory responses. By integrating insights from these regulatory mechanisms, there is potential to discover new therapeutic targets and potential biomarkers for early detection and management of Alzheimer’s disease. This review aims to enhance the understanding of the relationship between Alzheimer’s disease and non-coding RNAs, potentially paving the way for early detection and novel treatment strategies. Related Articles | Metrics

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Potential biofluid markers for cognitive impairment in Parkinson’s disease Jieyu Chen, Chunyu Liang, Fang Wang, Yongyun Zhu, Liuhui Zhu, Jianzhun Chen, Bin Liu, Xinglong Yang 2026, 21 (1):  281-295.  doi: 10.4103/NRR.NRR-D-24-00592 Abstract ( 62 )   PDF (2740KB) ( 18 )   Save Cognitive impairment is a particularly severe non-motor symptom of Parkinson’s disease that significantly diminishes the quality of life of affected individuals. Identifying reliable biomarkers for cognitive impairment in Parkinson’s disease is essential for early diagnosis, prognostic assessments, and the development of targeted therapies. This review aims to summarize recent advancements in biofluid biomarkers for cognitive impairment in Parkinson’s disease, focusing on the detection of specific proteins, metabolites, and other biomarkers in blood, cerebrospinal fluid, and saliva. These biomarkers can shed light on the multifaceted etiology of cognitive impairment in Parkinson’s disease, which includes protein misfolding, neurodegeneration, inflammation, and oxidative stress. The integration of biofluid biomarkers with neuroimaging and clinical data can facilitate the development of predictive models to enhance early diagnosis and monitor the progression of cognitive impairment in patients with Parkinson’s disease. This comprehensive approach can improve the existing understanding of the mechanisms driving cognitive decline and support the development of targeted therapeutic strategies aimed at modifying the course of cognitive impairment in Parkinson’s disease. Despite the promise of these biomarkers in characterizing the mechanisms underlying cognitive decline in Parkinson’s disease, further research is necessary to validate their clinical utility and establish a standardized framework for early detection and monitoring of cognitive impairment in Parkinson’s disease. Related Articles | Metrics

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Reprogramming induced neurons from olfactory ensheathing glial cells: A feasible approach for spinal cord injury repair Javier Sierra , María Portela-Lomba, Diana Simón, M. Teresa Moreno-Flores 2026, 21 (1):  296-297.  doi: 10.4103/NRR.NRR-D-24-01043 Abstract ( 40 )   PDF (1216KB) ( 15 )   Save Every year, around the world, between 250,000 and 500,000 people suffer a spinal cord injury (SCI). SCI is a devastating medical condition that arises from trauma or disease-induced damage to the spinal cord, disrupting the neural connections that allow communication between the brain and the rest of the body, which results in varying degrees of motor and sensory impairment. Disconnection in the spinal tracts is an irreversible condition owing to the poor capacity for spontaneous axonal regeneration in the affected neurons. This is due to several causes: (i) intrinsic neuronal deficits in the expression of genes involved in axon regrowth/regeneration; (ii) the presence of inhibitory factors as well as the lack of trophic factors for neuroprotection and regeneration in the affected area; and (iii) a physical impediment due to the formation of the glial scar (Varadarajan et al., 2022).  Related Articles | Metrics

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Spinal cord injury–associated disruption of the autonomic immune control: Does biological sex matter? Sara Rito-Fernandes, António J. Salgado, Nuno A. Silva, Susana Monteiro 2026, 21 (1):  298-299.  doi: 10.4103/NRR.NRR-D-24-01078 Abstract ( 33 )   PDF (1206KB) ( 9 )   Save The impact of spinal cord injury (SCI) on the immune system is increasingly recognized in a field traditionally focused on motor impairments. SCI can seriously affect the immune system by progressively disrupting the regulatory mechanisms that control immune responses. This dysregulation varies widely among patients and can evolve over time, ranging from systemic inflammatory responses to immunosuppression, greatly contributing to the morbidity and mortality of individuals with SCI (Bao et al., 2011; Brennan et al., 2024). Pro-inflammatory mediators produced at the site of injury not only instigate intraspinal inflammation by promoting the influx of peripheral leukocytes into the injured spinal cord, but also enter the bloodstream, triggering a systemic inflammatory response. Systemic inflammatory response is characterized by the activation and mobilization of circulating inflammatory cells, mainly neutrophils, which can infiltrate unaffected peripheral organs. The resulting pro-inflammatory microenvironment established within these tissues can lead to organ damage and dysfunction (Bao et al., 2011). When this dysregulation affects lymphoid organs, it can further exacerbate SCIassociated complications by causing secondary immunosuppression, resulting in increased vulnerability to infections (Brennan et al., 2024). Related Articles | Metrics

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Extra-pineal melatonin in perisynaptic Schwann cell–muscle fiber cross talk at the regenerating neuromuscular junction Samuele Negro, Cesare Montecucco, Michela Rigoni 2026, 21 (1):  300-301.  doi: 10.4103/NRR.NRR-D-24-01136 Abstract ( 36 )   PDF (1019KB) ( 12 )   Save The neuromuscular junction and its proregenerative niche: The mammalian peripheral nervous system, unlike the central nervous system, has preserved throughout evolution the ability to regenerate and fully restore function. Key factors for effective nerve regeneration include a supportive neuronal environment and a coordinated tissue response (Brosius Lutz and Barres, 2014) Related Articles | Metrics

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Cognition, apathy, and gait dysfunction in cerebral small vessel disease: A shared neural basis? Hao Li, Mengfei Cai, Anil Man Tuladhar 2026, 21 (1):  302-303.  doi: 10.4103/NRR.NRR-D-24-00925 Abstract ( 30 )   PDF (446KB) ( 22 )   Save Cerebral small vessel disease (SVD) represents a range of pathological changes in the small blood vessels of the brain. SVD can be detected on MRI, which includes white matter hyperintensities, lacunes, and cerebral microbleeds (Duering et al., 2023). Patients with SVD exhibit significant clinical heterogeneity, often presenting with cognitive impairment, apathy, gait dysfunction, and lacunar stroke (Wardlaw et al., 2019). The chronic and progressive symptoms, such as cognitive and motor complaints, as well as mood disorders, continuously affect SVD patients. This, in turn, often results in a loss of functional independence and a diminished quality of life (Wardlaw et al., 2019). Previous studies have focused on unraveling the underlying mechanisms, the trajectory, and the potential clinical outcomes of these specific symptoms (e.g., cognitive impairment, apathy, and gait dysfunction) in SVD (Wardlaw et al., 2019). However, these studies typically investigated each symptom individually, without integrating these symptoms to provide a comprehensive understanding. Related Articles | Metrics

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Uncovering optogenetic and chemogenetic induction of cognitive deficits: Efficient techniques for manipulating and observing specific neural activities Kyoungho Suk 2026, 21 (1):  304-305.  doi: 10.4103/NRR.NRR-D-24-00903 Abstract ( 30 )   PDF (607KB) ( 6 )   Save The hippocampus is part of the brain limbic system and plays an important role in learning and memory. Moreover, its ability to form, consolidate, and retrieve different types of memories makes it a central component in the cognitive functions necessary for everyday life. Understanding the role of the hippocampus helps comprehend how memories are created, stored, and recalled and sheds light on the impact of hippocampal damage in conditions such as Alzheimer’s disease and other forms of dementia. Optogenetics and chemogenetics are powerful tools that have been used to investigate the role of the hippocampus in learning and memory by allowing precise control and manipulation of specific neural circuits within the brain. While optogenetics utilizes light pulses to control light-sensitive ion channels (opsins), chemogenetics employs a designer drug to modulate designer receptors exclusively activated by the designer drug. These tools have significantly advanced our understanding of the role of the hippocampus in learning and memory by enabling researchers to unravel the complex interactions within the hippocampus that underlie cognitive functions. Further, these techniques allow researchers to manipulate and observe the effects of specific neural activities, thereby providing a deeper understanding of the mechanisms through which the hippocampus supports learning, memory formation, and recall. Related Articles | Metrics

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Aerobic exercise–induced myokine irisin release: A novel strategy to promote neuroprotection and improve cognitive function Jae-Won Choi, Rengasamy Balakrishnan 2026, 21 (1):  306-307.  doi: 10.4103/NRR.NRR-D-24-01034 Abstract ( 52 )   PDF (1045KB) ( 12 )   Save Challenges in the prevention and treatment of mild cognitive impairment associated with Alzheimer’s disease: Increased life expectancy due to advancements in medical care has given rise to an aging population, accompanied by a surge in the incidence of incurable neurodegenerative diseases (NDDs). These diseases primarily affect the cognitive and behavioral functions of older adults by impacting brain activity. Mild cognitive impairment (MCI) is a neurodegenerative condition that affects a significant portion of the population. Characterized by memory loss, MCI is believed to be an early indication of Alzheimer’s disease (AD) and is generally considered to be a transitional state between healthy aging and AD onset. Currently, 24 million people worldwide are affected by AD, a number projected to increase fourfold by 2050. By this date, the global population over 65 years is expected to be triple what it was in 2010, at nearly 1.5 billion individuals. While cognitive and behavioral impairment are the first clinical symptoms of AD, memory loss typically appears before clinical diagnosis—particularly in people over 65 years of age—due to progressive loss of neurons and synapses, mainly in the cortex and hippocampus. By the time, AD is clinically diagnosed, several pathological changes in the brain are already in progress, including oxidative stress, amyloid-β (Aβ) and tau protein accumulation, metabolism alterations, blood–brain barrier dysfunction, microbiotagut-brain axis dysfunction, mitochondrial dysfunction, and neuronal apoptosis. In pathological studies, excessive neuroinflammatory response and injury lead to the depletion of neurons in terms of structure, function, or quantity, resulting in the impairment of learning, memory, and other cognitive functions. These effects result in the early stages of MCI, which is associated with AD (Amartumur et al., 2024). Related Articles | Metrics

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Microglia and macrophages in brain injury and repair after subarachnoid hemorrhage David C. Lauzier , Harry V. Vinters, Shino D. Magaki 2026, 21 (1):  308-309.  doi: 10.4103/NRR.NRR-D-24-01037 Abstract ( 27 )   PDF (790KB) ( 10 )   Save Subarachnoid hemorrhage (SAH) is a devastating condition that affects a total of 8 million people worldwide each year (Lauzier and Athiraman, 2024). Etiologies of SAH can be traumatic or nontraumatic, with the majority of non-traumatic SAH occurring due to intracranial aneurysm rupture (Rutledge et al., 2014). Patients with poor outcomes from SAH often survive the acute phase and go on to deteriorate in a delayed fashion from secondary brain injury induced by cascades of injury initiated by aneurysm rupture. Practice-level improvements such as dedicated neurocritical care units, rapid treatment protocols harnessing infrastructure from ischemic stroke care, and standardization of nimodipine therapy have resulted in improved outcomes for patients with SAH. Despite these advances, the morbidity of SAH remains unacceptably high, and novel therapeutic targets must be identified. Related Articles | Metrics

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Gut microbiota modulates oligodendrocyte lineage cell response after traumatic brain injury Kirill Shumilov, Stuart Friess 2026, 21 (1):  310-311.  doi: 10.4103/NRR.NRR-D-24-01061 Abstract ( 31 )   PDF (1231KB) ( 15 )   Save Traumatic brain injury (TBI) is a significant public health issue, affecting approximately 1.7 million people annually in the United States alone, with over 5 million experiencing long-term disabilities (Roozenbeek et al., 2013). A major sequela of TBI is long-lasting white matter injury (WMI) which includes traumatic axonal injury and loss of myelination, resulting in cognitive, behavioral, and psychiatric deficits in survivors. To date, there are no effective therapies for traumatic WMI, and novel therapeutic approaches are urgently needed. Oligodendrocytes, which provide metabolic support to axons and are the producers of myelin in the central nervous system (CNS), undergo apoptosis after TBI, triggered by direct injury or in response to axonal degeneration (Flygt et al., 2016, 2017). Mature oligodendrocytes present in the brain at the time of injury have limited, if any, capability to contribute to remyelination. Therefore, the bulk of CNS remyelination is attributed to the differentiation of oligodendrocyte progenitor cells (Franklin and Ffrench-Constant, 2017), which can be adversely impacted by inflammation after TBI. This highlights that initial WMI from TBI is amplified by a failure of post-injury reparative mechanisms. Understanding the molecular and cellular mechanisms by which inflammation impairs oligodendrocyte progenitor cell proliferation and remyelination is thus essential to identify targetable post-injury processes to improve recovery. Related Articles | Metrics

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Shared mechanisms and pathological phenotypes underlying aminoacyl-tRNA synthetase-related neuropathies Elena R. Rhymes, James N. Sleigh 2026, 21 (1):  312-313.  doi: 10.4103/NRR.NRR-D-24-01080 Abstract ( 52 )   PDF (2480KB) ( 12 )   Save C h a r c o t- M a r i e - To o t h d i s e a s e ( C M T ) i s a heterogeneous group of inherited peripheral neuropathies; it is characterized by muscle weakness and wasting, as well as sensory dysfunction, that typically begins during adolescence and ultimately leads to lifelong disability. Occurring in ~1 in 2500 individuals, CMT is the most common hereditary neuromuscular condition and results from mutations in > 100 different genes. CMT is grouped into type 1 (CMT1), where demyelination and loss of nerve conduction velocity occur, type 2 (CMT2), where motor and sensory axons degenerate without loss of myelination/nerve conduction velocity, and intermediate CMT, where both demyelination and axon loss present alongside intermediate nerve conduction velocities. Related Articles | Metrics

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Base and translation of β-glucocerebrosidase and its transporter LIMP-2 in neuropathies Philipp Arnold , Friederike Zunke 2026, 21 (1):  314-315.  doi: 10.4103/NRR.NRR-D-24-01056 Abstract ( 29 )   PDF (1138KB) ( 8 )   Save The lysosomal enzyme β-glucocerebrosidase (GCase) belongs to the family of glycosidases and hydrolyses the glycosphingolipid glucosylceramide (GluCer) into glucose and ceramide. The enzyme is of central importance for two pathologies: (1) the lysosomal storage disorder Gaucher’s disease (GD) and (2) the neurodegenerative disorder Parkinson’s disease (PD). GCase is encoded by the gene GBA1 and mutations within GBA1 are the monogenetic cause for GD. This rare lysosomal storage disorder (overall global incidence 0.45–25.0 per 100,000 with high geographical and ethnical variations being more common in the Eastern world and among the Ashkenazi Jewish community with an estimated frequency of 1 in 1000) presents with high heterogeneity (Goker-Alpan and Ivanova, 2024). Due to the accumulation of GluCer, the substrate of GCase, common manifestations include enlarged liver and/or spleen (hepato-/ splenomegaly), anemia, thrombocytopenia as well as skeletal malformations. GD is classified in three types, which are distinguished by the presence and extent of neurological symptoms, including seizures, cognitive impairment, and spasticity (type I: non-neuronopathic; type II: acute neuronopathic; type III: chronic neuronopathic) (Beutler, 2001). Most GD cases (~90%) are related to type I caused by mild GBA1 variants (e.g., N370S). Severe variants (e.g., L444P) are more likely to lead to GD type II or III. All forms of GD are inherited in an autosomal recessive manner. The gold standard for treatment of GD type I is enzyme replacement therapy by regular intravenous administration of recombinant GCase (e.g., Imiglucerase) to overcome peripheral symptoms, such as organomegaly. Related Articles | Metrics

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A novel generation of potent gamma-secretase modulators: Combat Alzheimer’s disease and Down syndrome–associated Alzheimer’s disease Xu-Qiao Chen 2026, 21 (1):  316-317.  doi: 10.4103/NRR.NRR-D-24-00918 Abstract ( 28 )   PDF (4507KB) ( 11 )   Save Alzheimer’s disease and Down syndrome: Down syndrome (DS) is a genetic disorder caused by the presence of an extra complete or partial chromosome 21. Over the past few decades, significant advancements in medical treatment and nursing care have greatly improved the life expectancy of individuals with DS. However, as they age, their risk of developing Alzheimer’s disease (AD) increases considerably (Antonarakis et al., 2020). While DS patients experience multiple complications affecting various organs and systems due to developmental defects present from birth, AD remains a critical factor that significantly limits their lifespan. Consequently, delaying or even controlling the onset and progression of AD in DS is a crucial objective for potential drug development targeting this population. Related Articles | Metrics

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P2X7 receptors and multiple sclerosis: A potential biomarker and therapeutic target? Cristina Agliardi, Franca Rosa Guerini , Mario Clerici 2026, 21 (1):  318-319.  doi: 10.4103/NRR.NRR-D-24-01115 Abstract ( 47 )   PDF (1554KB) ( 14 )   Save Multiple sclerosis (MS) is a chronic, autoimmune and neuroinflammatory disease of the central nervous system (CNS) with a neurodegenerative component, characterized by demyelination and degeneration of nerve fibers. It affects mainly young adults (aged 20 to 45 years) and its causes are still unknown, but it is thought that external factors such as viruses and environmental factors trigger the disease in people with a genetic susceptibility. Patients are classified into four main categories based on the clinical course of the disease: relapsing remitting (RR)-MS, the most common form, characterized by relapses and periods of remission; secondary progressive (SP)-MS, which may develop secondarily in RR-MS patients, characterized by continuous worsening with or without periods of remission; primary progressive (PP)-MS in which symptoms continue to worsen from the onset of the disease. In particular, the PP-MS form is more resistant to the currently available pharmacological treatments used to treat the other forms, and progressive relapsing-MS, a rare form characterized by continuous disease progression from the onset. Related Articles | Metrics

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Alpha-synuclein-induced upregulation of SKI family transcriptional corepressor 1: A new player in aging and Parkinson’s disease? Lauren Barrett , Rebekah Bevans , Aideen M. Sullivan, Louise M. Collins, Gerard W. O’Keeffe 2026, 21 (1):  320-321.  doi: 10.4103/NRR.NRR-D-24-01156 Abstract ( 30 )   PDF (478KB) ( 8 )   Save SKI family transcriptional corepressor 1 (SKOR1; also known as LbxCor1, Fussel15, or CORL1), is a member of the SKI family of proteins and is transcribed from a protein-coding gene located on chromosome 15 in humans, that has a molecular weight of approximately 100 kDa. Skor1 is highly expressed in neurons in the central nervous system of both humans and rodents. It has been shown to regulate the transcription of genes that are involved in pathways related to restless legs syndrome (RLS) (Sarayloo et al., 2020), and SKOR1 genetic variants have been associated with RLS (Jimenez-Jimenez et al., 2018). RLS is a common neurological condition that has a strong genetic component, with many cases being linked to hereditary factors; RLS often occurs secondary to other medical conditions including neuropathies such as Parkinson’s disease (PD) (Ondo et al., 2002). Related Articles | Metrics

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Potential treatment of Alzheimer’s disease astrocyte pathology based on nuclear lipid regulation Masato Komai, Nobumasa Takasugi 2026, 21 (1):  322-323.  doi: 10.4103/NRR.NRR-D-24-01125 Abstract ( 28 )   PDF (1091KB) ( 9 )   Save The purpose of this perspective is to discuss the future development of a potential treatment of glial pathology in Alzheimer’s disease (AD) and a new regulatory mechanism, nuclear lipids, which may be involved in the pathogenesis of the disease, based on the work of the authors (Takasugi et al., 2011; Komai et al., 2024). Related Articles | Metrics

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Positive impact of indicaxanthin from Opuntia ficusindica fruit on high-fat diet–induced neuronal damage and gut microbiota dysbiosis Simona Terzo, Antonella Amato, Pasquale Calvi, Marta Giardina, Domenico Nuzzo, Pasquale Picone, Antonio Palumbo-Piccionello, Sara Amata, Ilenia Concetta Giardina, Alessandro Massaro, Ignazio Restivo, Alessandro Attanzio, Luisa Tesoriere, Mario Allegra, Flavia Mulè 2026, 21 (1):  324-332.  doi: 10.4103/NRR.NRR-D-23-02039 Abstract ( 47 )   PDF (5548KB) ( 32 )   Save Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet; the high-fat diet group was fed a high-fat diet; and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally (0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet–induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids (Lachnospiraceae, Alloprovetella, and Lactobacillus), and by reducing bacteria related to unhealthy profiles (Blautia, Faecalibaculum, Romboutsia and Bilophila). In conclusion, indicaxanthin has a positive effect on high-fat diet–induced neuronal damage and on the gut microbiota composition in obese mice. Related Articles | Metrics

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Neuroserpin alleviates cerebral ischemia-reperfusion injury by suppressing ischemia-induced endoplasmic reticulum stress Yumei Liao, Qinghua Zhang, Qiaoyun Shi, Peng Liu, Peiyun Zhong, Lingling Guo, Zijian Huang, Yinghui Peng, Wei Liu, Shiqing Zhang, István Adorján, Yumi Fukuzaki, Eri Kawashita, Xiao-Qi Zhang, Nan Ma, Xiaoshen Zhang, Zoltán Molnár, Lei Shi 2026, 21 (1):  333-345.  doi: 10.4103/NRR.NRR-D-24-00044 Abstract ( 40 )   PDF (4744KB) ( 19 )   Save Neuroserpin, a secreted protein that belongs to the serpin superfamily of serine protease inhibitors, is highly expressed in the central nervous system and plays multiple roles in brain development and pathology. As a natural inhibitor of recombinant tissue plasminogen activator, neuroserpin inhibits the increased activity of tissue plasminogen activator in ischemic conditions and extends the therapeutic windows of tissue plasminogen activator for brain ischemia. However, the neuroprotective mechanism of neuroserpin against ischemic stroke remains unclear. In this study, we used a mouse model of middle cerebral artery occlusion and oxygen-glucose deprivation/reperfusion-injured cortical neurons as in vivo and in vitro ischemia-reperfusion models, respectively. The models were used to investigate the neuroprotective effects of neuroserpin. Our findings revealed that endoplasmic reticulum stress was promptly triggered following ischemia, initially manifesting as the acute activation of endoplasmic reticulum stress transmembrane sensors and the suppression of protein synthesis, which was followed by a later apoptotic response. Notably, ischemic stroke markedly downregulated the expression of neuroserpin in cortical neurons. Exogenous neuroserpin reversed the activation of multiple endoplasmic reticulum stress signaling molecules, the reduction in protein synthesis, and the upregulation of apoptotic transcription factors. This led to a reduction in neuronal death induced by oxygen/glucose deprivation and reperfusion, as well as decreased cerebral infarction and neurological dysfunction in mice with middle cerebral artery occlusion. However, the neuroprotective effects of neuroserpin were markedly inhibited by endoplasmic reticulum stress activators thapsigargin and tunicamycin. Our findings demonstrate that neuroserpin exerts neuroprotective effects on ischemic stroke by suppressing endoplasmic reticulum stress. Related Articles | Metrics

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Changes in border-associated macrophages after stroke: Single-cell sequencing analysis Ning Yu, Yang Zhao, Peng Wang, Fuqiang Zhang, Cuili Wen, Shilei Wang 2026, 21 (1):  346-356.  doi: 10.4103/NRR.NRR-D-24-01092 Abstract ( 61 )   PDF (19511KB) ( 7 )   Save Border-associated macrophages are located at the interface between the brain and the periphery, including the perivascular spaces, choroid plexus, and meninges. Until recently, the functions of border-associated macrophages have been poorly understood and largely overlooked. However, a recent study reported that border-associated macrophages participate in stroke-induced inflammation, although many details and the underlying mechanisms remain unclear. In this study, we performed a comprehensive single-cell analysis of mouse border-associated macrophages using sequencing data obtained from the Gene Expression Omnibus (GEO) database (GSE174574 and GSE225948). Differentially expressed genes were identified, and enrichment analysis was performed to identify the transcription profile of border-associated macrophages. CellChat analysis was conducted to determine the cell communication network of border-associated macrophages. Transcription factors were predicted using the ‘pySCENIC’ tool. We found that, in response to hypoxia, borderassociated macrophages underwent dynamic transcriptional changes and participated in the regulation of inflammatory-related pathways. Notably, the tumor necrosis factor pathway was activated by border-associated macrophages following ischemic stroke. The pySCENIC analysis indicated that the activity of signal transducer and activator of transcription 3 (Stat3) was obviously upregulated in stroke, suggesting that Stat3 inhibition may be a promising strategy for treating border-associated macrophages-induced neuroinflammation. Finally, we constructed an animal model to investigate the effects of border-associated macrophages depletion following a stroke. Treatment with liposomes containing clodronate significantly reduced infarct volume in the animals and improved neurological scores compared with untreated animals. Taken together, our results demonstrate comprehensive changes in border-associated macrophages following a stroke, providing a theoretical basis for targeting border-associated macrophages-induced neuroinflammation in stroke treatment. Related Articles | Metrics

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Empowering the NSC-34 cell line as a motor neuron model: Cytosine arabinoside’s action Giuseppe Vitale, Susanna Amadio, Francesco Liguori, Cinzia Volonté 2026, 21 (1):  357-364.  doi: 10.4103/NRR.NRR-D-24-00034 Abstract ( 48 )   PDF (22001KB) ( 3 )   Save The NSC-34 cell line is a widely recognized motor neuron model and various neuronal differentiation protocols have been exploited. Under previously reported experimental conditions, only part of the cells resemble differentiated neurons; however, they do not exhibit extensive and time-prolonged neuritogenesis, and maintain their duplication capacity in culture. The aim of the present work was to facilitate long-term and more homogeneous neuronal differentiation in motor neuron–like NSC-34 cells. We found that the antimitotic drug cytosine arabinoside promoted robust and persistent neuronal differentiation in the entire cell population. Long and interconnecting neuronal processes with abundant growth cones were homogeneously induced and were durable for up to at least 6 weeks in culture. Moreover, cytosine arabinoside was permissive, dispensable, and mostly irreversible in priming NSC-34 cells for neurite initiation and regeneration after mechanical dislodgement. Finally, the expression of the cell proliferation antigen Ki67 was inhibited by cytosine arabinoside, whereas the expression levels of neuronal growth associated protein 43, vimentin, and motor neuron–specific p75, Islet2, homeobox 9 markers were upregulated, as confirmed by western blot and/or confocal immunofluorescence analysis. Overall, these findings support the use of NSC-34 cells as a motor neuron model for properly investigating neurodegenerative mechanisms and prospectively identifying neuroprotective strategies. Related Articles | Metrics

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Microglia overexpressing brain-derived neurotrophic factor promote vascular repair and functional recovery in mice after spinal cord injury Fanzhuo Zeng, Yuxin Li, Xiaoyu Li Xinyang Gu, Yue Cao, Shuai Cheng, He Tian, Rongcheng Mei, Xifan Mei 2026, 21 (1):  365-376.  doi: 10.4103/NRR.NRR-D-24-00381 Abstract ( 37 )   PDF (90502KB) ( 14 )   Save Spinal cord injury represents a severe form of central nervous system trauma for which effective treatments remain limited. Microglia is the resident immune cells of the central nervous system, play a critical role in spinal cord injury. Previous studies have shown that microglia can promote neuronal survival by phagocytosing dead cells and debris and by releasing neuroprotective and anti-inflammatory factors. However, excessive activation of microglia can lead to persistent inflammation and contribute to the formation of glial scars, which hinder axonal regeneration. Despite this, the precise role and mechanisms of microglia during the acute phase of spinal cord injury remain controversial and poorly understood. To elucidate the role of microglia in spinal cord injury, we employed the colony-stimulating factor 1 receptor inhibitor PLX5622 to deplete microglia. We observed that sustained depletion of microglia resulted in an expansion of the lesion area, downregulation of brain-derived neurotrophic factor, and impaired functional recovery after spinal cord injury. Next, we generated a transgenic mouse line with conditional overexpression of brain-derived neurotrophic factor specifically in microglia. We found that brain-derived neurotrophic factor overexpression in microglia increased angiogenesis and blood flow following spinal cord injury and facilitated the recovery of hindlimb motor function. Additionally, brain-derived neurotrophic factor overexpression in microglia reduced inflammation and neuronal apoptosis during the acute phase of spinal cord injury. Furthermore, through using specific transgenic mouse lines, TMEM119, and the colony-stimulating factor 1 receptor inhibitor PLX73086, we demonstrated that the neuroprotective effects were predominantly due to brain-derived neurotrophic factor overexpression in microglia rather than macrophages. In conclusion, our findings suggest the critical role of microglia in the formation of protective glial scars. Depleting microglia is detrimental to recovery of spinal cord injury, whereas targeting brain-derived neurotrophic factor overexpression in microglia represents a promising and novel therapeutic strategy to enhance motor function recovery in patients with spinal cord injury. Related Articles | Metrics

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Chitosan alleviates symptoms of Parkinson’s disease by reducing acetate levels, which decreases inflammation and promotes repair of the intestinal barrier and blood– brain barrier Yinying Wang, Rongsha Chen, Guolin Shi, Xinwei Huang, Ke Li, Ruohua Wang, Xia Cao, Zhongshan Yang, Ninghui Zhao, Jinyuan Yan 2026, 21 (1):  377-391.  doi: 10.4103/NRR.NRR-D-23-01511 Abstract ( 40 )   PDF (21169KB) ( 1 )   Save Studies have shown that chitosan protects against neurodegenerative diseases. However, the precise mechanism remains poorly understood. In this study, we administered chitosan intragastrically to an MPTP-induced mouse model of Parkinson’s disease and found that it effectively reduced dopamine neuron injury, neurotransmitter dopamine release, and motor symptoms. These neuroprotective effects of chitosan were related to bacterial metabolites, specifically shortchain fatty acids, and chitosan administration altered intestinal microbial diversity and decreased short-chain fatty acid production in the gut. Furthermore, chitosan effectively reduced damage to the intestinal barrier and the blood–brain barrier. Finally, we demonstrated that chitosan improved intestinal barrier function and alleviated inflammation in both the peripheral nervous system and the central nervous system by reducing acetate levels. Based on these findings, we suggest a molecular mechanism by which chitosan decreases inflammation through reducing acetate levels and repairing the intestinal and blood–brain barriers, thereby alleviating symptoms of Parkinson’s disease. Related Articles | Metrics

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Long noncoding RNA GAS5 acts as a competitive endogenous RNA to regulate GSK-3β and PTEN expression by sponging miR-23b-3p in Alzheimer’s disease Li Zeng, Kaiyue Zhao, Jianghong Liu, Mimin Liu, Zhongdi Cai, Ting Sun, Zhuorong Li, Rui Liu 2026, 21 (1):  392-405.  doi: 10.4103/NRR.NRR-D-23-01273 Abstract ( 45 )   PDF (5847KB) ( 33 )   Save Long noncoding RNA and microRNA are regulatory noncoding RNAs that are implicated in Alzheimer’s disease, but the role of long noncoding RNA-associated competitive endogenous RNA has not been fully elucidated. The long noncoding RNA growth arrest-specific 5 (GAS5) is a member of the 5′-terminal oligopyrimidine gene family that may be involved in neurological disorders, but its role in Alzheimer’s disease remains unclear. This study aimed to investigate the function of GAS5 and construct a GAS5-associated competitive endogenous RNA network comprising potential targets. RNA sequencing results showed that GAS5 was upregulated in five familial Alzheimer’s disease (5×FAD) mice, APPswe/PSEN1dE9 (APP/PS1) mice, Alzheimer’s disease-related APPswe cells, and serum from patients with Alzheimer’s disease. Functional experiments with targeted overexpression and silencing demonstrated that GAS5 played a role in cognitive dysfunction and multiple Alzheimer’s disease-associated pathologies, including tau hyperphosphorylation, amyloid-beta accumulation, and neuronal apoptosis. Mechanistic studies indicated that GAS5 acted as an endogenous sponge by competing for microRNA-23b-3p (miR-23b-3p) binding to regulate its targets glycogen synthase kinase 3beta (GSK-3β) and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) expression in an Argonaute 2-induced RNA silencing complex (RISC)-dependent manner. GAS5 inhibited miR-23b-3p-mediated GSK-3β and PTEN cascades with a feedforward PTEN/protein kinase B (Akt)/GSK-3β linkage. Furthermore, recovery of GAS5/miR-23b-3p/GSK-3β/PTEN pathways relieved Alzheimer’s disease-like symptoms in vivo, indicated by the amelioration of spatial cognition, neuronal degeneration, amyloid-beta load, and tau phosphorylation. Together, these findings suggest that GAS5 promotes Alzheimer’s disease pathogenesis. This study establishes the functional convergence of the GAS5/miR-23b-3p/GSK-3β/PTEN pathway on multiple pathologies, suggesting a candidate therapeutic target in Alzheimer’s disease. Related Articles | Metrics

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Contribution of ferroptosis and SLC7A11 to lightinduced photoreceptor degeneration Xiaoxu Huang, Yumeng Zhang, Yuxin Jiang, Tong Li, Shiqi Yang, Yimin Wang, Bo Yu, Minwen Zhou, Guanran Zhang, Xiaohuan Zhao, Junran Sun, Xiaodong Sun 2026, 21 (1):  406-416.  doi: 10.4103/NRR.NRR-D-23-01741 Abstract ( 73 )   PDF (9587KB) ( 3 )   Save Progressive photoreceptor cell death is one of the main pathological features of age-related macular degeneration and eventually leads to vision loss. Ferroptosis has been demonstrated to be associated with retinal degenerative diseases. However, the molecular mechanisms underlying ferroptosis and photoreceptor cell death in age-related macular degeneration remain largely unexplored. Bioinformatics and biochemical analyses in this study revealed xC– , solute carrier family 7 member 11-regulated ferroptosis as the predominant pathological process of photoreceptor cell degeneration in a light-induced dry age-related macular degeneration mouse model. This process involves the nuclear factor-erythroid factor 2-related factor 2-solute carrier family 7 member 11-glutathione peroxidase 4 signaling pathway, through which cystine depletion, iron ion accumulation, and enhanced lipid peroxidation ultimately lead to photoreceptor cell death and subsequent visual function impairment. We demonstrated that solute carrier family 7 member 11 overexpression blocked this process by inhibiting oxidative stress in vitro and in vivo. Conversely, solute carrier family 7 member 11 knockdown or the solute carrier family 7 member 11 inhibitor sulfasalazine and ferroptosis-inducing agent erastin aggravated H2O2-induced ferroptosis of 661W cells. These findings indicate solute carrier family 7 member 11 may be a potential therapeutic target for patients with retinal degenerative diseases including age-related macular degeneration. Related Articles | Metrics