Cellular and Molecular Neurobiology最新文献

{"title":"Druggable Targets for Postpartum Depression: A Mendelian Randomization and Colocalization Study.","authors":"Song Wu, Meihong Shen, Huiyan Wang, Wenbo Zhou","doi":"10.1007/s10571-025-01581-x","DOIUrl":"10.1007/s10571-025-01581-x","url":null,"abstract":"<p><p>Postpartum depression (PPD) remains a complex disorder with poorly understood genetic underpinnings. This study systematically evaluated the genetic susceptibility of PPD and identified potential therapeutic targets using Mendelian Randomization (MR) approach. Using a two-sample MR approach, the study assessed the causal effects of expression quantitative trait loci (eQTLs) of druggable genes in blood on PPD, which was sourced from the FinnGen. The primary analytical method was the inverse variance weighted, supplemented by a series sensitivity analyses. Summary-data-based Mendelian Randomization (SMR) analysis was used to validate the identified genes, and Bayesian colocalization analysis evaluated shared causal variants and colocalization probabilities between significant targets and PPD. A Phenome-Wide Association Study (PheWAS) was conducted to assess the associations of established PPD markers with other traits to exclude potential side effects. The results showed that the eQTLs of 12 druggable genes were significantly associated with PPD susceptibility. Seven genes were identified as risk factors, and the expression levels of five genes significantly reduced PPD susceptibility. Colocalization analysis supported the hypothesis that PPD may be associated with shared causal variants of ALDH16A1 (OR = 1.09, 95% CI 1.05-1.13, PP.H4 = 0.78) and SLC29A4 (OR = 1.36, 95% CI 1.23-1.50, PP.H4 = 0.76). The PheWAS did not indicate potential side effects for these two therapeutic targets. This study identified new genetic susceptibilities and potential therapeutic targets associated with PPD, providing novel insights for clinical diagnosis and treatment, and offering new research directions for understanding the molecular mechanisms of PPD.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"61"},"PeriodicalIF":3.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12179039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Emotional Stress and Adaptive Behavior with Stroke Risk: A Mendelian Randomization Study.","authors":"Jianyu Liu, Chunlan Pu, Cao Liu, Qiang Zhou, Da Liu, Tianqi Lu, Zhouyang Liu, Xing Guo, Hua Liu","doi":"10.1007/s10571-025-01577-7","DOIUrl":"10.1007/s10571-025-01577-7","url":null,"abstract":"<p><p>Although emotional stress and adaptive behavior are known to influence cardiovascular health, direct evidence linking them to stroke remains limited. This study aims to clarify the associations between emotional stress, adaptive behaviors, and the risk of stroke. We conducted a two-sample Mendelian randomization analysis using data from the UK Biobank, the European Bioinformatics Institute, the Integrative Epidemiology Unit, and the FinnGen project. Indirect effects were estimated using the product of coefficients method. Low satisfaction with family relationships was associated with increased risks of all stroke and ischemic stroke. Mood swings were linked to higher risks of all stroke, ischemic stroke, and large-artery stroke, while feelings of tension were associated with large-artery stroke and small vessel stroke. Interestingly, nervousness was inversely associated with intracerebral hemorrhage risk. Participation in group leisure activities was associated with reduced risks of all stroke, ischemic stroke, and small vessel stroke. In contrast, several adaptive behaviors were linked to increased stroke risk, including vigorous physical activity (all stroke), summer outdoor activities (all stroke and ischemic stroke), winter outdoor activities (all stroke), and prolonged television watching (all stroke, ischemic stroke, and large-artery stroke). Mediation analyses suggested that hypertension, type 2 diabetes, atherosclerotic heart disease, and chronic ischemic heart disease may partially mediate these associations. The study provides genetic evidence supporting a potential causal relationship between emotional stress, adaptive behaviors, and stroke subtypes. Individuals can easily modify adaptive behaviors and manage emotional stress in their daily routines. Understanding these associations may inform future strategies for stroke prevention; however, due to limitations inherent in the current study design, our findings require further validation in large-scale prospective cohort studies.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"59"},"PeriodicalIF":3.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Senolytic Treatment Attenuates Global Ischemic Brain Injury and Enhances Cognitive Recovery by Targeting Mitochondria.","authors":"Caihong Gu, Ting Guo, Xiaobing Chen, Xinyu Zhou, Yong Sun","doi":"10.1007/s10571-025-01580-y","DOIUrl":"10.1007/s10571-025-01580-y","url":null,"abstract":"<p><p>The benefits of senolytic therapy have been known in a series of age-related diseases, whereas its potential roles in global cerebral ischemic (GCI) brain injury remain unexplored. In current study, we aim to investigate the effects of combined senolytics Dasatinib plus Quercetin (D&Q) treatment in GCI and the underlying mechanisms in a mouse model. We firstly report that 12-week post-GCI D&Q treatment effectively eliminated cellular senescence of astrocytes and microglia in the hippocampus of mice brain, followed by decreased release of the potent inflammatory senescence-associated secretory phenotypes (SASP). Further mechanistic analysis suggested that D&Q administration can effectively regulate mitochondrial function as a critical downstream target. D&Q treatment inhibited GCI-induced mitochondrial fragmentation and maintained mitochondrial integrity. Subsequently, D&Q treatment improved the mitochondrial metabolic function by enhancing mitochondrial cytochrome c oxidase (CCO) activity and ATP production. Moreover, D&Q treatment reversed the decline of mitochondrial antioxidant enzyme SOD2 and reduced the ROS accumulation and suppressed oxidative damage to cellular protein structure. Further investigation indicated D&Q treatment protected the hippocampal neurons after GCI by mitigating the dendritic injury and neuronal apoptotic signaling. Extensive behavioral tests assessed the functional outcomes and showed that D&Q treatment effectively preserved hippocampus-dependent spatial reference memory and recognition memory, and mitigated GCI-induced anxiety and depression levels. Taken together, our study provides leading evidence for the neuroprotective roles of the senolytics D&Q in GCI model and identifies regulation of mitochondrial functions could be the key underlying mechanism. These findings offer novel insights into the potential clinical applications of senolytic agents in therapy.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"60"},"PeriodicalIF":3.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12177126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Nuclear Receptors on the Progression of Multiple Sclerosis: A Review.","authors":"Behina Babaalizadeh, Fatemeh Kalaki-Jouybari, Fatemeh Abarghooi-Kahaki, Hamed Afkhami, Zahra-Sadat Razavi","doi":"10.1007/s10571-025-01563-z","DOIUrl":"10.1007/s10571-025-01563-z","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is the consequence of early-onset inflammatory demyelination and progressive neurodegenerative lesions in the central nervous system (CNS). Despite the unclear pathogenesis of MS, two main processes occur, oligodendrocyte repair and lipid metabolism. Nuclear receptors have been observed to have a role as ligand sensors, regulators of transcriptional factors, and modulators of gene expression. One member of this family, the retinoid X receptor (RXR), which forms a heterodimeric complex with liver X receptor (LXR), have been implicated in the pathophysiology of MS. Moreover, it has been expressed that LXR receptors play pivotal role in the regulation of inflammation, oxidative stress responses, and cholesterol metabolism in phagocytes in active MS lesions. This review aimed to study role of RXR and LXR in MS pathogenesis.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"58"},"PeriodicalIF":3.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyroptosis in Alzheimer's Disease: Mechanisms and Therapeutic Potential.","authors":"Tian Tang","doi":"10.1007/s10571-025-01579-5","DOIUrl":"10.1007/s10571-025-01579-5","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid plaques, neurofibrillary tangles (NFTs), and neuroinflammation. Recent research has revealed that pyroptosis, an inflammatory programmed cell death (PCD), plays a crucial role in AD pathology. The pyroptosis signaling cascade triggered by β-amyloid (Aβ) and hyperphosphorylated tau protein leads to the release of proinflammatory cytokines, forming a \"neuroinflammation-neurodegeneration\" vicious cycle. Therapeutic strategies targeting the pyroptosis signaling pathway show promise, with evidence suggesting that inhibition of inflammasomes, caspase-1, or gasdermin D (GSDMD) can alleviate AD-related pathological features. However, the specificity of the existing inhibitors is insufficient, and research on non-classical pyroptosis pathway remains in its early stages. More mechanisms and therapeutic strategies targeting pyroptosis-related pathway need to be explored to enhance the therapeutic efficacy. Targeting the pyroptosis pathway provides a novel direction for AD treatment. Exploring and summarizing its mechanisms along with the clinical translational applications of targeted inhibitors will offer fresh perspectives for moving beyond traditional \"symptom control\" therapies and achieving \"pathology-modifying\" interventions, holding significant scientific and clinical importance.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"57"},"PeriodicalIF":3.6,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174016/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astroglial Kir4.1 and AQP4 Channels: Key Regulators of Potassium Homeostasis and Their Implications in Autism Spectrum Disorders.","authors":"Vesal Abbasian, Shima Davoudi, Amin Vahabzadeh, Mohammad Javad Maftoon-Azad, Mahyar Janahmadi","doi":"10.1007/s10571-025-01574-w","DOIUrl":"10.1007/s10571-025-01574-w","url":null,"abstract":"<p><p>Astroglial Kir4.1 and AQP4 channels are pivotal regulators of potassium (K⁺) and water homeostasis in the brain, playing essential roles in maintaining neuronal stability, facilitating synaptic transmission, and supporting overall brain function. Kir4.1 channels promote the efficient uptake of K⁺ ions from the extracellular space, particularly during periods of high neuronal activity, thereby preventing excessive neuronal excitability-a condition linked to several neurological disorders, including Autism Spectrum Disorder (ASD). Meanwhile, AQP4 channels, predominantly expressed in the astrocytic end-feet at the blood-brain barrier, regulate water transport across cell membranes, ensuring osmotic balance that complements the function of Kir4.1 in K⁺ clearance. Recent studies have underscored the critical link between dysfunctions in these channels and the pathophysiology of ASD, a complex neurodevelopmental disorder characterized by a broad range of social, communicative, and behavioral impairments. Mutations or dysregulations in Kir4.1 and AQP4 channels can disrupt K⁺ and water homeostasis, exacerbating neuronal hyperexcitability and contributing to hallmark ASD symptoms, such as sensory processing abnormalities, social deficits, and an increased risk of seizures. This review synthesizes current findings, focusing on the molecular mechanisms of Kir4.1 and AQP4 channels, their role in astrocyte-neuron interactions, and their pathophysiological implications in ASD. It also provides a detailed discussion of potential therapeutic interventions targeting these channels to mitigate ASD symptoms.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"56"},"PeriodicalIF":3.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12158897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibrinogen and Complement Factor H Induce Parkinsonian and Cognitive Impairment-Like Features in Mice.","authors":"Aditi Naskar, Mahesha Sachin, Senjuti Sengupta, Pallavi Bhadrachalam, Shantala Hegde, Ravi Yadav, Pramod Kumar Pal, Phalguni Anand Alladi","doi":"10.1007/s10571-025-01576-8","DOIUrl":"10.1007/s10571-025-01576-8","url":null,"abstract":"<p><p>Cognitive impairment is one of the non-motor symptoms of Parkinson's disease (PD), which may precede motor impairment. Biomarker(s) can help detect the cognitive dysfunction, much earlier in the disease and may differentiate PD patients with and without cognitive impairments. Animal model-based biomarker validation studies can provide better insights into pathogenesis and open up avenues for addressing therapeutics; however, such studies using non-genetic modalities, are few. Our earlier non-targeted label-free proteomics-assisted biomarker study on CSF of PD patients with cognitive impairment (PDCI), revealed the presence of elevated levels of fibrinogen and complement factor H (CFAH) in PDCI-CSF. We now intend to determine if these proteins harbor a pathogenic potential, when present above physiological levels. Native fibrinogen and recombinant CFAH were intraperitoneally injected in adult C57BL/6J mice and 48 h later the motor and cognitive behavior alongside neuroanatomical correlates were studied. The motor and cognitive deficits were complemented by degenerative changes in the SNpc, striatum, CA1 and subiculum in the injected mice. The altered gut microarchitecture suggests the possibility of other non-motor symptoms. Here, we show that fibrinogen and CFAH can potentially induce motor, and non-motor deficits in mice, akin to the PDCI-associated neuropathological deficits, and thus are potential biomarkers.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"54"},"PeriodicalIF":3.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypercholesterolemia Duration and Brain Area Determine Inflammatory Response Intensity and Apoptotic Mediator Activation in Apo E^-/-/LDLR^-/- Double-Knockout Mice.","authors":"Ewelina Czuba-Pakuła, Jolanta Ochocińska, Sebastian Głowiński, Alicja Braczko, Ryszard T Smoleński, Grażyna Lietzau, Przemysław Kowiański","doi":"10.1007/s10571-025-01562-0","DOIUrl":"10.1007/s10571-025-01562-0","url":null,"abstract":"<p><p>Hypercholesterolemia (Hch) is a risk factor for cerebrovascular and neurodegenerative diseases, manifesting with symptoms that vary depending on damage to specific brain regions. Hch triggers inflammatory responses and cell death. However, the progression of these processes in relation to the duration of Hch and the location of pathology in the central nervous system remains unclear. Therefore, we aimed to investigate (1) the impact of age and duration of Hch on neuroinflammatory responses and programmed cell death in the brain and (2) the intensity of these processes in various brain areas during Hch. In this study, we used 3-, 6-, and 12-month-old male Apo E^-/-/LDLR^-/- double-knockout mice and age-matched wild-type C57BL/6 mice (control group). Concentrations of cytokines IL-1β, IL-4, and IL-6, as well as apoptotic mediators AIF and Cas-3, were measured using enzyme-linked immunosorbent assay in the whole brain and separately in the prefrontal cortex (PFCx), hippocampus (HIP), and striatum (STR). The results showed that the Hch-induced release of cytokines IL-1β and IL-6, decreased expression of IL-4, and elevated level of apoptotic markers AIF and Cas-3 correlated with Hch duration. The inflammatory response and expression of apoptotic markers were more pronounced in the HIP and STR compared to the PFCx. Our results indicate a correlation between the neurodegenerative effects of Hch and its duration and highlight the varying susceptibility of different brain areas to Hch-induced damage.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"55"},"PeriodicalIF":3.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoplasmic Reticulum Stress Inhibition Promotes Mitophagy via Miro1 Reduction to Rescue Mitochondrial Dysfunction and Protect Dopamine Neurons in Parkinson's Disease.","authors":"Yuqi Wen, Zheng Han, Bao Wang, Chenxi Feng, Xvshen Ding, Yangni Li, Yan Lv, Xuelian Wang, Li Gao","doi":"10.1007/s10571-025-01575-9","DOIUrl":"10.1007/s10571-025-01575-9","url":null,"abstract":"<p><p>Both mitochondrial dysfunction and endoplasmic reticulum stress (ERS) have been implicated in the pathogenesis of Parkinson's disease (PD). However, the underlying regulatory mechanisms between ERS and mitochondrial dysfunction remain unclear. In the present study, we found that an in vitro model of Parkinson's disease (PD) induced by methyl-4-phenylpyridine (MPP⁺) showed increased intracellular peroxidation, leading to a significant increase in ERS. ER staining and immunofluorescence analysis of ERS-related proteins verified the presence of ERS, whereas transmission electron microscopy (TEM) showed complete depletion of ER. Notably, treatment with 4-phenylbutyric acid (4-PBA) to suppress ERS reduced apoptosis and concurrently reversed the ER micromorphology. Furthermore, 4-PBA alleviated mitochondrial dysfunction, as shown by increased mitochondrial membrane potential (MMP), upregulation of electron transport chain proteins, and restoration of mitochondrial integrity. Further studies revealed that the effect of 4-PBA could be attributed to the modulation of the mitochondrial Rho-GTPase 1 (Miro1)-mitophagy axis. In vivo experiments in Parkinson's disease models demonstrated that inhibiting ERS reduced dopaminergic neuron loss while improving cognitive and motor function. Collectively, these findings indicate that treatments targeting ERS may be potential candidates for treating PD.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"53"},"PeriodicalIF":3.6,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12122992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polymer-Based Electrochemical Sensors for the Diagnosis of Neurodegenerative Diseases.","authors":"Qitong Zhang, Guangran Zhao, Shilin Wang, Yuxuan Song, Yuanzheng Sun","doi":"10.1007/s10571-025-01570-0","DOIUrl":"10.1007/s10571-025-01570-0","url":null,"abstract":"<p><p>Acute and chronic neurodegenerative diseases (NDs), including multiple sclerosis (MS), Alzheimer's disease (AD), and Parkinson's disease (PD), are characterized by neurodegeneration, which is the gradual malfunction and damage of neurons and axons in the central nervous system. Improved clinical diagnostic workups and the development and tracking of successful disease-modifying treatments are made possible by detecting appropriate neurodegenerative disease (ND) biomarkers. Important biomarkers, such as Tau proteins, amyloid-β, and α-synucleins, are essential for precise identification but are often evaluated using time-consuming, expensive, and traditional techniques like polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Due to its exceptional selectivity and sensitivity, electrochemical biosensing has become a popular, low-cost substitute for more conventional diagnostic methods. Nanoparticles in biosensors are particularly noteworthy because they improve electron transport and aid in immobilizing biorecognition components. Conducting polymers have shown great potential in the field of electrochemical sensing. Conducting polymers have shown great potential in electrochemical sensing. Additionally, research has shown that polypyrrole, polyaniline, poly(3,4-ethylenedioxythiophene), and poly(thiophene) are often regarded as among the best conducting polymers for fabricating electrochemical sensors. Moreover, a hydrogel biosensor allows for the detection of many parameters simultaneously with real-time monitoring, allowing for more accurate and timely tracking of multiple indicators of a patient. Hydrogel nano(bio)composite sensors that use electrochemical transduction methods to detect analytes are also available. Hydrogel-based polymer sensors for early-stage neurodegenerative diagnosis are examined in this review in a novel way. Afterward, we reviewed electrochemical sensors developed for detecting biomarkers related to diseases, including multiple sclerosis, Alzheimer's, Parkinson's, and Huntington's. There have also been developments devised to enhance efficacy of electrochemical diagnostic tools to address their limitations. In this respect, we have also reviewed many polymers used in electrochemical diagnosis of neurological disorders. Finally, we have also evaluated the limits and prospects of clinical trials involving these electrochemical means of diagnoses.</p>","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"52"},"PeriodicalIF":3.6,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12106273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}