Degenerative neurological and neuromuscular disease最新文献

{"title":"TP73-AS1 Regulates MPP+-Induced Cell Inflammation and Apoptosis in SH-SY5Y Cells.","authors":"Xue Zhang, Li Xue, Haiyan Li, Xiaolong Yu, Kaixin Dou, Anmu Xie","doi":"10.2147/DNND.S539895","DOIUrl":"10.2147/DNND.S539895","url":null,"abstract":"<p><strong>Background: </strong>The aim was to investigate the potential role of TP73-AS1 in the pathogenesis of Parkinson's disease.</p><p><strong>Methods: </strong>Peripheral blood samples were obtained from three patients with early-onset Parkinson's disease (PD), three patients with late-onset PD, and three healthy controls for the extraction of total RNA. Genomic long non-coding RNA (lncRNA) expression levels were analyzed using the Illumina HiSeq2500 sequencing platform. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to study the expression of TP73-AS1. Flow cytometry and Western blot analyses were conducted to assess the functional role of TP73-AS1 in SH-SY5Y cells in vitro. Moreover, the expression of inflammatory cytokines, such as IL-16, IL-6, and α-synuclein (SYN), was examined using cellular immunofluorescence techniques.</p><p><strong>Results: </strong>Among early-onset PD patients, 59 lncRNAs were significantly upregulated, and 57 lncRNAs were significantly downregulated compared to the control group. Similarly, late-onset PD patients showed 70 upregulated lncRNAs and 77 downregulated lncRNAs with statistical significance compared to the control group. In vitro studies indicated a significant increase in lncRNA TP73-AS1 expression in the MPP+-treated group in contrast with the control group (<i>P</i> < 0.001). Furthermore, the MPP+-treated group displayed elevated levels of Cleaved caspase-3, IL-16, as well as IL-6 (<i>P</i> < 0.001). Conversely, Bcl-2 expression decreased, Bax expression increased, and the Bax/Bcl-2 expression ratio demonstrated an increase (<i>P</i> < 0.001). Reducing lncRNA TP73-AS1 resulted in decreased apoptosis and inflammation, along with a decrease in α-SYN expression (<i>P</i> < 0.001). Notably, the absence of TP73-AS1 showed a protective effect against PD, suggesting it to be a potential target for the treatment of PD. These findings suggest that TP73-AS1 may serve as a potential molecular marker for the early diagnosis of PD, providing a new perspective for understanding the regulatory mechanisms of inflammation and apoptosis in PD.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"15 ","pages":"81-94"},"PeriodicalIF":3.2,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12420920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manganese-Induced Parkinsonism: A Review of Etiologies and Treatments.","authors":"Nitish M Khindri, Mary C Maj","doi":"10.2147/DNND.S482018","DOIUrl":"10.2147/DNND.S482018","url":null,"abstract":"<p><p>Parkinson's disease is a neurodegenerative disorder that leads to neuronal loss. Though a variety of genetic and environmental factors may be involved in the etiology, the presentation of the disorder is very similar. Trace minerals such as manganese are essential for brain development and function though effective concentrations are paramount. Exposure to high concentrations of manganese is known to cause neurotoxicity and has been recently associated with manganese-induced parkinsonism, which will be explored in this review. This review synthesizes findings from peer-reviewed clinical, epidemiological, and experimental studies to explore the underlying mechanisms and contributing factors of manganese-induced parkinsonism. Specifically, it examines alterations in lipidomic and oxidative profiles, enhancement of redox cycling, transporter dysfunction and deficiency, ion homeostasis, dysregulation of signaling pathways and autophagy, mRNA disruption, dopamine toxicity, manganese contamination, and neuroprotective mechanisms. Preventative and therapeutic interventions-including chelation therapy with ethylene-diamine-tetra-acetic acid (CaNa₂EDTA), with or without plasma exchange and para-aminosalicylic acid (PAS), as well as natural compounds such as vinpocetine (VIN), punicalagin (PUN), niacin, vitamin E, DNLA, curcumin, and sesame oil-are also reviewed. Given manganese's role as an oxidant in the synthesis of neurotoxic compounds, therapeutic strategies targeting both manganese, its associated molecular pathways, and its downstream neurotoxic effects may represent the most promising direction for future research.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"15 ","pages":"65-79"},"PeriodicalIF":2.1,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Based on the Dual Pathway of Interaction-Mediated NF-κB in Cell Apoptosis and Immune Inflammation to Study the Effect of Danzhi Xiaoyao Powder on the Learning and Cognitive Ability of AD Model Rats.","authors":"Hu-Ping Wang, Ming-Cheng Li, Jiao Yang, Jun Zhou, Zhi-Peng Meng, Yun-Yun Hu, Yu-Jie Lyu, Yi-Qin Chen, Yu-Mei Han, Wen-Li Pei","doi":"10.2147/DNND.S475290","DOIUrl":"https://doi.org/10.2147/DNND.S475290","url":null,"abstract":"<p><strong>Background: </strong>Apoptosis and immune inflammation play important roles in the pathological process of Alzheimer's disease (AD), but their specific pathogenesis is still unclear. Therefore, this article focuses on exploring the effects of Danzhi Xiaoyao Powder (DXP) on the learning and memory ability of AD model rats from the dual mechanisms of apoptosis and immune inflammation.</p><p><strong>Methods: </strong>The AD model was replicated by injecting Okadaic acid (100 ng) into the bilateral hippocampus of rats. Successful rats were selected and orally administered with donepezil hydrochloride and DXP decoction for 42 days. Their learning and memory abilities, hippocampal morphology, Aβ expression, inflammatory factors, apoptotic factors, anti apoptotic factors, as well as the expression of pathway proteins and mRNA were detected.</p><p><strong>Results: </strong>After DXP intervention, the learning and memory abilities of rats improved, the neuronal cell arrangement was more complete, the expression of Aβ decreased, the expression of pro-inflammatory cytokine and apoptotic factors decreased, the expression of anti apoptotic factors increased, Protein Kinase B (Akt) expression and activity significant up-regulation, and nuclear factor kappa-B (NF-κB), p38 MAPK (p38), MAPKAPK-2 (MK2), Cyclooxygenase-2 (COX-2) protein and mRNA expression were significantly down-regulated.</p><p><strong>Conclusion: </strong>DXP can improve the learning and cognitive abilities of AD model rats, and its mechanism of action may be related to the regulation of the Akt/NF-κB apoptosis pathway mediated by NF-κB interaction and the p38MAPK/MK2/COX-2 immune inflammatory dual pathway.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"15 ","pages":"41-64"},"PeriodicalIF":2.1,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12035751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144059978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene Editing for Duchenne Muscular Dystrophy: From Experimental Models to Emerging Therapies.","authors":"Umme Sabrina Haque, Toshifumi Yokota","doi":"10.2147/DNND.S495536","DOIUrl":"https://doi.org/10.2147/DNND.S495536","url":null,"abstract":"<p><p>The CRISPR system has emerged as a ground-breaking gene-editing tool, offering promising therapeutic potential for Duchenne muscular dystrophy (DMD), a severe genetic disorder affecting approximately 1 in 5000 male births globally. DMD is caused by mutations in the dystrophin gene, which encodes a critical membrane-associated protein essential for maintaining muscle structure, function and repair. Patients with DMD experience progressive muscle degeneration, loss of ambulation, respiratory insufficiency, and cardiac failure, with most succumbing to the disease by their third decade of life. Despite the well-characterized genetic basis of DMD, curative treatments- such as exon skipping therapies, micro-dystrophin, and steroids- remain elusive. Recent preclinical studies have demonstrated the promise of CRISPR-based approaches in restoring dystrophin expression across various models, including human cells, murine systems, and large animal models. These advancements highlight the potential of gene editing to fundamentally alter the trajectory of the disease. However, significant challenges persist, including immunogenicity, off-target effects, and limited editing efficiency, which hinder clinical translation. This review provides a comprehensive analysis of the latest developments in CRISPR-based therapeutic strategies for DMD. It emphasizes the need for further innovation in gene-editing technologies, delivery systems, and rigorous safety evaluations to overcome current barriers and harness the full potential of CRISPR/Cas as a durable and effective treatment for DMD.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"15 ","pages":"17-40"},"PeriodicalIF":2.1,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12002074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Hypothesized Therapeutic Role of (Z)-Endoxifen in Duchenne Muscular Dystrophy (DMD).","authors":"H Lawrence Remmel, Sandra S Hammer, Laurence A Neff, Olivier M Dorchies, Leonardo Scapozza, Dirk Fischer, Steven C Quay","doi":"10.2147/DNND.S496904","DOIUrl":"10.2147/DNND.S496904","url":null,"abstract":"<p><p>Duchenne Muscular Dystrophy (DMD) is an inherited, X-linked disorder that is progressive, debilitating, and ultimately fatal. The current therapeutic landscape offers no cures, but does include palliative treatments that delay disease progression, and there is progress on genetic therapies that have the promise to be curative. There is much room for new therapies, and foundational work with the estrogen receptor modulator tamoxifen suggests the potential of a unique spectrum of therapeutic benefit from endoxifen, a metabolite of tamoxifen. Here we describe the potential for this new DMD therapy in the context of the overall DMD therapeutic landscape.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"15 ","pages":"1-15"},"PeriodicalIF":2.1,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cold Inducible RNA-Binding Protein Promotes the Development of Alzheimer's Disease Partly by Inhibition of uPA in Astrocytes.","authors":"Ze Li, Jing Peng Liu, Feng Hua Yao, Yang Cao, Shou Chun Li, Yuan Yang Liu, Su Xin Wen, Yu Xiao Liu, Ai Jun Liu","doi":"10.2147/DNND.S490526","DOIUrl":"10.2147/DNND.S490526","url":null,"abstract":"<p><strong>Background: </strong>Cold inducible RNA-binding protein (CIRP) is an important danger-associated molecular pattern involved in tissue-specific and systemic inflammation related to inflammation and Alzheimer's disease (AD). However, the precise roles and mechanism of CIRP in the functional changes in astrocytes during the development of AD are still unknown. This study aimed to assess gene expression alterations in astrocytes after they overexpress CIRP (oe-CIRP) and to explore the relationship between abnormal CIRP expression and AD.</p><p><strong>Methods: </strong>We created astrocyte cell lines with a CIRP or control vector expression using three human glioma cell lines U87, U251 and H4, and analyzed the mRNA expression profiles of 3 pairs of cells via microarray. Bioinformatics identified differentially expressed mRNAs between CIRP-overexpressing (ov-CIRP) and control groups, validated by q-PCR and Western blotting (WB). Finally, the effect of CIRP overexpression in astrocytes on neurons was observed in a coculture system.</p><p><strong>Results: </strong>We identified 119 mRNAs with obvious fold changes between the ov-CIRP and control groups for all 3 pairs of human glioma cell lines. The biological functional analysis indicated that urokinase plasminogen activator (uPA), a gene whose expression significantly decreased after CIRP overexpression, was closely associated with AD. WB and q-PCR confirmed that CIRP overexpression significantly inhibited uPA at both mRNA and protein levels in U87, U251 and H4 cells. Moreover, compared with those cocultured with control astrocytes, SH-SY5Y cells cocultured with CIRP-overexpressing astrocytes exhibited a significant increase in the expression of amyloid-β (Aβ)1-42 and the hyperphosphorylated microtubule-associated protein tau (Tau).</p><p><strong>Conclusion: </strong>CIRP overexpression in astrocytes inhibits uPA expression, promoting Aβ1-42 production and tau phosphorylation in neurons, thereby increasing AD risk. These results suggest that the overexpression of CIRP in astrocytes contributes to the development of AD.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"14 ","pages":"143-155"},"PeriodicalIF":2.1,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11687300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoinjectors for Administering Glatiramer Acetate in Relapsing Remitting Multiple Sclerosis in Europe: A Survey of Patient and Nurse Preferences.","authors":"Santosh B Shirol, Riyaz Ahmed Saboor, Thomas Müller","doi":"10.2147/DNND.S484306","DOIUrl":"10.2147/DNND.S484306","url":null,"abstract":"<p><strong>Purpose: </strong>Multiple sclerosis (MS) is a neurological disorder affecting almost 2.8 million people globally, approximately 80-85% of whom have the relapsing-remitting form of the disease (RRMS). There are several autoinjectors available for the administration of injectable disease-modifying therapies for the treatment of MS. The objective of the current study was to gain an understanding of factors related to patients' and nurses' autoinjector preferences, and to evaluate two autoinjectors for glatiramer acetate (MyJECT™ and CSYNC™) against those preferences.</p><p><strong>Patients and methods: </strong>Patients with RRMS and nurses experienced in training patients with an autoinjector were recruited from 12 health centers in Germany. Surveys were administered to patients and nurses and their answers to 13 questions over five categories (participants' characteristics, important autoinjector attributes, autoinjector performance, satisfaction with the autoinjector devices and demographics) were scored, where appropriate, using a 5-point Likert scale.</p><p><strong>Results: </strong>A total of 15 patients and 15 nurses were included in the study. Overall, the top four most important attributes, for both nurses and patients, were ease of handling, ability to use independently, ease of gripping the autoinjector and ease of self-injection. MyJECT™ received a mean score of at least 4.5 (out of 5) on more attributes than CSYNC™ and satisfaction with both autoinjectors was high.</p><p><strong>Conclusion: </strong>Nurses and patients with RRMS were highly satisfied with both the MyJECT™ and CSYNC™ autoinjectors, with scores suggesting that MyJECT™ performs better on the attributes they identified as most important. All patients currently using the MyJECT™ were likely or highly likely to recommend it to another patient with RRMS.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"14 ","pages":"131-141"},"PeriodicalIF":2.1,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Transcriptome Analysis Reveals Molecular Subtypes and ceRNA Networks in Multiple Sclerosis.","authors":"Caili Ji, Li Ding, Fumin Jia, Zhiyong Zhang, Cong Long","doi":"10.2147/DNND.S491211","DOIUrl":"10.2147/DNND.S491211","url":null,"abstract":"<p><strong>Aim: </strong>Multiple sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system (CNS). While extensively studied, its molecular subtypes and mechanisms remain poorly understood, hindering the identification of effective therapeutic targets.</p><p><strong>Methods: </strong>We used ConsensusClusterPlus to analyze transcriptome data from 215 MS patient samples, identifying distinct molecular subtypes. Differential expression analysis and variability assessments were conducted to further characterize these subtypes. Additionally, circular RNAs (circRNAs) and microRNAs (miRNAs) were screened for potential ceRNA interactions.</p><p><strong>Results: </strong>Three molecular subtypes were identified: MS-<i>FCRL1</i> (C1), MS-<i>BTG1</i> (C2), and MS-<i>RPL38</i> (C3). Each subtype was involved in key MS-related pathways (as annotated by KEGG), but the core genes regulating these pathways differed significantly among the subtypes. Subtype C3 exhibited neurodegenerative pathway enrichment, increased immune activity, and immune cell infiltration, suggesting a more severe disease course. Further analysis revealed 18 differentially expressed circRNAs and 22 miRNAs, with <i>EEF1D</i> and <i>TUBA1A</i> as hub targets in C3.</p><p><strong>Discussion: </strong>Differential activation of immune pathways across MS subtypes suggests specific gene expression drives disease heterogeneity. We propose a circ_0045537/miR-196a-5p/<i>TUBA1A</i> axis in subtype C3, modulating microtubule dynamics and worsening MS severity.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"14 ","pages":"115-130"},"PeriodicalIF":2.1,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11669277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study on the Effects of Acupuncture with the \"Yizhi Tiaoshen\" Acupoint Formula on Blood Oxygen Metabolism and Neural Function in Key Brain Regions of AD Rats.","authors":"Ren-Zhen Zhang, Xin Zhang, Tian-Tian Zhu, Yu-Juan Ye, Ming-Li Su, Yu-Ting Wei, Xing-Ke Yan","doi":"10.2147/DNND.S468770","DOIUrl":"https://doi.org/10.2147/DNND.S468770","url":null,"abstract":"<p><strong>Purpose: </strong>Exploring the effects of acupuncture at the \"Yizhi Tiaoshen\" acupoint on blood oxygen metabolism and neurological function changes in the brain regions of AD model rats.</p><p><strong>Methods: </strong>The AD model was replicated by intraperitoneal injection of D-galactose combined with bilateral hippocampal CA1 injection of Okadaic acid (OA). Thirty rats with successfully replicated model were selected through Morris water maze experiment and randomly divided into model group, donepezil hydrochloride group, and acupuncture group, with 10 rats in each group. After treatment, fNIRs were used to detect changes in Oxy Hb, Deoxy Hb, and Total Hb in the cerebral cortex of rats in each group, in order to evaluate the neurological function changes in key brain areas.</p><p><strong>Results: </strong>The escape latency of the donepezil hydrochloride group and the acupuncture group was shortened, the number of crossings through the original platform increased, and the duration of stay in the quadrant where the original platform was located was prolonged. Based on fNIRs detection, the main differential channels of blood oxygen metabolism in AD rats were identified as 2-2 and 8-7, corresponding to the prefrontal and parietal lobes, respectively. The concentrations of Oxy Hb and Total Hb were significantly increased in both treatment groups, while the concentration of Deoxy Hb was significantly decreased.</p><p><strong>Conclusion: </strong>Acupuncture with the \"Yizhi Tiaoshen\" acupoint formula and donepezil hydrochloride can improve the learning and memory function of AD rats, and its mechanism may be related to improving blood oxygen metabolism in the prefrontal and parietal regions and protecting neuronal function.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"14 ","pages":"103-114"},"PeriodicalIF":2.1,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11410027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142304522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in Blood Biomarkers for Alzheimer's Disease: Ultra-Sensitive Detection Technologies and Impact on Clinical Diagnosis.","authors":"Yi Zhang, Kefan Bi, Linfu Zhou, Jie Wang, Lingtong Huang, Yan Sun, Guoping Peng, Wei Wu","doi":"10.2147/DNND.S471174","DOIUrl":"10.2147/DNND.S471174","url":null,"abstract":"<p><p>Alzheimer's disease has escalated into a critical public health concern, marked by its neurodegenerative nature that progressively diminishes cognitive abilities. Recognized as a continuously advancing and presently incurable condition, AD underscores the necessity for early-stage diagnosis and interventions aimed at delaying the decline in mental function. Despite the proven efficacy of cerebrospinal fluid and positron emission tomography in diagnosing AD, their broader utility is constrained by significant costs and the invasive nature of these procedures. Consequently, the innovation of blood biomarkers such as Amyloid-beta, phosphorylated-tau, total-tau et al, distinguished by their high sensitivity, minimal invasiveness, accessibility, and cost-efficiency, emerges as a promising avenue for AD diagnosis. The advent of ultra-sensitive detection methodologies, including single-molecule enzyme-linked immunosorbent assay and immunoprecipitation-mass spectrometry, has revolutionized the detection of AD plasma biomarkers, supplanting previous low-sensitivity techniques. This rapid advancement in detection technology facilitates the more accurate quantification of pathological brain proteins and AD-associated biomarkers in the bloodstream. This manuscript meticulously reviews the landscape of current research on immunological markers for AD, anchored in the National Institute on Aging-Alzheimer's Association AT(N) research framework. It highlights a selection of forefront ultra-sensitive detection technologies now integral to assessing AD blood immunological markers. Additionally, this review examines the crucial pre-analytical processing steps for AD blood samples that significantly impact research outcomes and addresses the practical challenges faced during clinical testing. These discussions are crucial for enhancing our comprehension and refining the diagnostic precision of AD using blood-based biomarkers. The review aims to shed light on potential avenues for innovation and improvement in the techniques employed for detecting and investigating AD, thereby contributing to the broader field of neurodegenerative disease research.</p>","PeriodicalId":93972,"journal":{"name":"Degenerative neurological and neuromuscular disease","volume":"14 ","pages":"85-102"},"PeriodicalIF":2.1,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11297492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}