Current Alzheimer research最新文献

{"title":"Exploring the Mechanism of Saponins from Panax japonicus in Improving Alzheimer's Disease Based on Network Pharmacology and Molecular Docking.","authors":"Qi-Qi Huang, Xue-Li Zhang, Shu-Jing He, Yi-Han Zhou, Ting Wang, Chun-Xia Zhang","doi":"10.2174/0115672050471394260327075445","DOIUrl":"https://doi.org/10.2174/0115672050471394260327075445","url":null,"abstract":"<p><strong>Introduction: </strong>To study the mechanism of saponins from Panax japonicus (SPJ) in improving Alzheimer's disease based on network pharmacology and molecular docking technology.</p><p><strong>Methods: </strong>The active components in the SPJ were obtained from the databases of CNKI, PubMed, and PubChem. The active component targets were retrieved from the databases of Swiss Target Prediction and Super-PRED. The disease targets were retrieved from the databases GeneCards, OMIM, and PharmGKB. Drug-disease intersection targets were obtained via Venny 2.1.0. The String database was utilized to establish the protein network. The drug- active ingredient- target network was constructed by Cytoscape 3.10.1 software. The Metascape database was employed to conduct the gene ontology function enrichment analysis and KEGG pathway enrichment analysis. AutoDock Tools 1.5.7 was used to perform the molecular docking analysis.</p><p><strong>Results: </strong>A total of 57 active components were obtained from the SPJ, and 438 drug targets and 2294 disease targets were identified, including 169 identical targets. The key targets were SRC, STAT3, PIK3R1, AKT1, ESR1, EGFR, and JUN. Pseudoginsenoside F11, Vina-ginsenoside R2, and Chikusetsusaponin III might be the key active components of SPJ in improving Alzheimer's disease. The key active components showed good binding energy and better binding affinity within the active targets.</p><p><strong>Discussion: </strong>Network pharmacology has screened out 57 potential active components of SPJ, including pseudo ginsenoside F11, ginsenoside R2, and III, which may exert therapeutic effects by acting on key targets such as SRC, STAT3, PIK3R1, AKT1, ESR1, EGFR, and JUN. These targets are closely related to core pathological processes of AD, such as Aβ production, Tau protein phosphorylation, neuroinflammation, neuronal survival, and synaptic plasticity. Functional analysis indicates that SPJ may act on multiple cellular sites, such as receptor complexes and synaptic membranes, by influencing biological processes such as cell migration, inflammatory response, and membrane potential regulation. Pathway enrichment suggests that its mechanism of action may be related to Alzheimer's disease pathways, the NF-κB signaling pathway, and the calcium signaling pathway. The continuous activation of NF-κB can exacerbate neuroinflammation and oxidative damage, while the disorder of the calcium signaling pathway will lead to intracellular calcium overload, mitochondrial dysfunction, and synaptic damage, all of which play key roles in the progression of AD.</p><p><strong>Conclusion: </strong>SPJ exerts a therapeutic effect and provides the basis for Alzheimer's disease through multiple components, targets, and pathways.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147978271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alzheimer's Disease: Silent Erosion of Memory - From Discovery to Modern Crisis and the Quest for a Cure.","authors":"Rasheed M A Q Jamhour, Haya Ayyal Salman, Mohammed Alshammari, Afaf F Almuqati, Mohamed H Fayed, Ghassab M Al-Mazaideh","doi":"10.2174/0115672050423446251215051844","DOIUrl":"https://doi.org/10.2174/0115672050423446251215051844","url":null,"abstract":"<p><p>Alzheimer's Disease (AD) is a progressive neurodegenerative disorder characterized by a decline in cognitive abilities and memory impairment, representing the most common form of dementia worldwide. First described by Alois Alzheimer in 1906, AD continues to pose significant global health and socioeconomic challenges, with incidence anticipated to exceed 14 million cases by 2060. Despite decades of investigation, the specific pathophysiology -comprising multifactorial mechanisms such as genetic predisposition, environmental influences, lifestyle factors, amyloid-β (Aβ) plaques, neurofibrillary tangles, tau pathology, as well as vascular disease - remains incompletely understood. This review provides a comprehensive summary of the current knowledge regarding these mechanisms, and it explores the field's new therapeutic modalities, such as monoclonal antibodies, ultrasound-based treatments, and novel diagnostic tools based on biomarkers. It also discusses the socioeconomic burden of AD and regional challenges in the Middle East, as well as the impact of the COVID-19 pandemic on dementia care. While many of AD's underlying causes are aggressive and difficult to treat, new research in genetics, natural compounds, and groundbreaking therapies offers hope for better diagnosis and treatment. Above all, this study emphasizes the importance of having more effective chemotherapeutic or radiological approaches for ADs, as well as a robust medical system capable of providing these treatments to the patients.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149070808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Ectopic Fat in Alzheimer's Disease.","authors":"Ye Yang, Xueyan Huang, Hexu Liu, Changyin Yu","doi":"10.2174/0115672050461650260406064722","DOIUrl":"https://doi.org/10.2174/0115672050461650260406064722","url":null,"abstract":"<p><p>Alzheimer's Disease (AD) is a neurodegenerative disorder increasingly recognized to be associated with metabolic dysfunction. Accumulating evidence suggests that ectopic fat (abnormal fat deposition in non-adipose tissue) is a key factor. This review summarizes the crucial role that ectopic fat plays in the onset and progression of AD, as well as the interrelated pathways through which ectopic fat deposition promotes the pathological process of AD. Adipocytes have been reported to produce and secrete amyloid-β (Aβ), a hallmark pathological feature of AD. Accordingly, ectopic fat may aggravate cerebral Aβ accumulation by impairing peripheral Aβ clearance. In addition, ectopic fat can also cause Insulin Resistance (IR), adipokine dysregulation, inflammatory responses, and oxidative stress. Therefore, ectopic fat is closely associated with the progression of AD and may play a contributory role in its pathogenesis. The effects of ectopic fat on the occurrence and development of Alzheimer's Disease (AD) pathology were reviewed through mechanisms such as metabolic disorders, inflammatory pathways, and Aβ deposition, and potential intervention strategies for this harmful cycle were highlighted. As current therapies for AD remain limited, new opportunities for its prevention and treatment may be provided through a better understanding of these associations.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Shared Mechanisms in Atherosclerosis and Alzheimer's Disease.","authors":"Devesh B Chaudhari, Kalyani Barve","doi":"10.2174/0115672050447493260327074829","DOIUrl":"https://doi.org/10.2174/0115672050447493260327074829","url":null,"abstract":"<p><p>Atherosclerosis and Alzheimer's Disease are two significant health concerns characterised by overlapping pathophysiological mechanisms, including chronic inflammation, oxidative stress, and lipid metabolism dysregulation. Impaired vascular integrity in atherosclerosis enhances the accumulation of Aβ plaque in the brain by reducing cerebral perfusion and compromising the clearance of Aβ. This review examines the shared pathways linking these conditions, emphasizing the role of the NLRP3 inflammasome, Receptor for Advanced Glycation End Products, and the apolipoprotein E4 allele in exacerbating vascular dysfunction that promotes neurodegeneration. The interplay between these factors underscores the potential of targeting these common pathways as a therapeutic strategy for both diseases. In preclinical studies, emerging treatments, NLRP3 inflammasome inhibitors like MCC950 and CY-09, show promise in mitigating both arterial plaque formation and neuronal amyloid deposition, while innovative microRNA-based therapies targeting miR-146a and miR-155 offer novel approaches to reduce inflammatory responses. Additionally, modulation of lipid metabolism through liver X receptor agonists like T0901317 and cholesteryl ester transfer protein inhibitors, including Anacetrapib, offers potential dual benefits for cardiovascular and neurological health. However, challenges such as restricted BBB permeability, genetic and sex variability, and limited long-term clinical evidence continue to constrain the effectiveness of dual-targeted therapeutic approaches. Future perspectives suggest integrating multi-- modal therapies that combine anti-inflammatory, lipid-regulatory, and antioxidant strategies to effectively address these interrelated diseases. Advancements in molecular biology and imaging techniques may facilitate the development of personalised medicine approaches, ultimately improving outcomes for patients suffering from both atherosclerosis and Alzheimer's Disease.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Efficacy and Safety of Cholinesterase Inhibitors and NMDA Receptor Antagonists in Alzheimer's Disease: A Systematic Review and Network Meta-Analysis of Randomized Controlled Trials.","authors":"Yulian Li, Luo Li, Qiao Yang, JianZhong Xiong","doi":"10.2174/0115672050437623260417063631","DOIUrl":"https://doi.org/10.2174/0115672050437623260417063631","url":null,"abstract":"<p><strong>Introduction: </strong>The study aims to evaluate and rank cholinesterase inhibitors, the NMDA antagonist memantine, anti-amyloid monoclonal antibodies, and non-drug modalities with respect to cognitive outcomes, functional status, neuropsychiatric symptoms, and tolerability.</p><p><strong>Methodology: </strong>We registered a protocol in PROSPERO and searched PubMed/MEDLINE, Embase, CENTRAL, Web of Science, trial registries, and gray literature through June 2025. Eligible randomized phase II/III trials in adults with clinically diagnosed AD were screened in duplicate. Data on interventions, comparators, outcomes (e.g., MMSE, ADAS-Cog, CDR-SB), and adverse events were extracted. Risk of bias was assessed using Cochrane RoB 2. A Bayesian random-effects NMA synthesized 125 trials (n > 30,000), estimating standardized Mean Differences (SMDs) with 95% Credible Intervals (CrIs). Heterogeneity (I²) and inconsistency (design-by-treatment, node-splitting) were evaluated.</p><p><strong>Results: </strong>The network was well connected, with low-to-moderate heterogeneity (global I² = 38.5%) and no significant inconsistency (p = 0.48). Cognitive training (SMD = 0.45; 95% CrI 0.30-0.60; SUCRA 92%), aerobic exercise (SMD = 0.55; 95% CrI 0.35-0.75; SUCRA 87%), and galantamine (SMD = 0.40; 95% CrI 0.22-0.58; SUCRA 84%) ranked highest versus placebo. Donepezil (SMD = 0.21; 95% CrI 0.11-0.30; SUCRA 78%) and memantine (SMD = 0.24; 95% CrI 0.13-0.35; SUCRA 72%) showed modest benefits.</p><p><strong>Discussion: </strong>Risk-of-bias ratings were low in 37% of trials, some concerns in 48%, and high in 15%. Subgroup analyses confirmed greater cholinesterase inhibitor efficacy in mild AD and superior memantine effects in moderate-to-severe disease.</p><p><strong>Conclusion: </strong>Non-pharmacological interventions demonstrated short-term cognitive benefits primarily in mild Alzheimer's disease populations and should be interpreted as adjunctive symptomatic strategies rather than direct substitutes for pharmacological therapy.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut Microbiota Dysbiosis in Alzheimer's Disease and Possible Therapeutic Options.","authors":"Rakesh Kumar Nayak, Soumya Ranjan Mohapatra, Satyam Kumar Sahoo, Susanta Kumar Sahu, Bimalendu Chowdhury, Zeenath Banu, Nihar Ranjan Das","doi":"10.2174/0115672050448298260303052535","DOIUrl":"https://doi.org/10.2174/0115672050448298260303052535","url":null,"abstract":"<p><p>Human microbiota consists of trillions of microbial cells dominated by bacteria, which live in the human body, while the term microbiome refers to the collective genetic material of microorganisms. Among them, the gut microbiota has emerged as pivotal, producing its own metabolites, neurotransmitter precursors, and immune mediators that affect brain development and function. These signals function via the complex, bidirectional Gut-Brain Axis (GBA). This is a communication network that connects the gastrointestinal tract to the central nervous system. This axis plays an important role in the regulation of gastrointestinal homeostasis, neurodevelopment, emotional regulation, and cognitive processes. Increasing evidence suggests that microbial dysbiosis within the gastrointestinal tract is involved in the pathogenesis and progression of several neurological and neurodegenerative disorders, including mood disorders, schizophrenia, autism spectrum disorder, Alzheimer's Disease (AD), Parkinson's Disease (PD), and Huntington's Disease. These insights have opened new therapeutic possibilities, and multiple microbiota-targeted interventions, such as dietary modification, prebiotics, probiotics, postbiotics, psychobiotics, antibiotics, and Fecal Microbiota Transplantation (FMT), are now being explored for their therapeutic value, especially in Alzheimer's disease.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral Hyperperfusion with Lecanemab in Alzheimer's Disease Assessed by Amyloid PET and Arterial Spin Labeling.","authors":"Naoya Imai, Hirohito Yano, Yuka Ikegame, Shoji Yasuda, Ryo Morishima, Ayumi Okumura, Morio Kumagai, Jun Shinoda, Tsuyoshi Izumo","doi":"10.2174/0115672050453079260226065149","DOIUrl":"https://doi.org/10.2174/0115672050453079260226065149","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Alzheimer's Disease (AD) is characterized by cognitive decline, amyloid-β deposition, and decreased Cerebral Blood Flow (CBF). Lecanemab, a monoclonal antibody targeting amyloid-β, slows cognitive decline in AD; however, its effects on CBF remain unclear. This study aimed to characterize CBF changes following lecanemab treatment and their association with baseline amyloid burden.</p><p><strong>Methods: </strong>Thirty patients with AD treated with lecanemab were analyzed retrospectively. Baseline amyloid deposition was quantified using the Centiloid scale, and patients were stratified into low, middle, and high groups. CBF was analyzed at baseline and at 8, 12, and 26 weeks using arterial spin labeling (ASL). Monoclonal antibody-triggered cerebral hyperperfusion (MATCH) was defined as a >20% CBF increase at week 8.</p><p><strong>Results: </strong>Seven patients were MATCH-positive (median CBF: 133.5% [125.5-167.8] of baseline). All MATCH-positive patients exhibited a decrease in CBF at week 12 compared to week 8. MATCH occurred in 6 of 10 patients in the middle Centiloid group. The low Centiloid group showed stable CBF, while the high Centiloid group showed a decreasing trend. The MATCHpositive group showed a significant deterioration in Instrumental Activities of Daily Living scores.</p><p><strong>Discussion: </strong>A transient CBF increase was closely associated with the middle Centiloid group. These CBF responses, including MATCH, may reflect amyloid removal, hyperperfusion, amyloidrelated imaging abnormalities, or immune responses.</p><p><strong>Conclusions: </strong>CBF changes differed according to baseline amyloid burden. Understanding these therapy-related CBF changes is crucial for elucidating AD pathology, and ASL provides a practical, non-invasive method for longitudinal CBF monitoring in routine clinical practice.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148261104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An Inverse Association Between the Composite Dietary Antioxidant Index and Alzheimer's Disease: Evidence from an NHANES-Based Cross-Sectional Study.","authors":"Yuxin Zhang, Shu Tong, Yan Chen, Chen Li, Yinhui Yao, Shiying Tang, Yazhen Shang","doi":"10.2174/0115672050462427260407045906","DOIUrl":"https://doi.org/10.2174/0115672050462427260407045906","url":null,"abstract":"<p><strong>Introduction: </strong>The relationship between the dietary Complex Antioxidant Index (CDAI) and Alzheimer's Disease (AD) is not clear. Our study is to investigate the relationship between CDAI and the risk of AD in general adults.</p><p><strong>Methods: </strong>This study included 116876 participants from the National Health and Nutrition Survey (NHANES). CDAI was calculated based on the intake of six dietary antioxidants. We used multivariate logistic regression to examine the relationship between CDAI and AD prevalence, and used restricted cubic splines to examine the nonlinear association.</p><p><strong>Results: </strong>The study showed that in the multivariate logistic regression model with fully adjusted confounding variables, the odds ratio (OR) of CDAI and AD was 0.9983 (95% confidence interval: 0.9969,0.9998; P=0.024). In addition, restricted cubic spline analysis revealed a linear correlation (P for non-linearity = 0.097).</p><p><strong>Discussion: </strong>This cross-sectional study reveals a linear negative association between the CDAI and AD prevalence in U.S. adults, with vitamin E, carotenoids, and selenium showing independent protective effects. These findings align with the hypothesis that dietary antioxidants may mitigate oxidative stress-related neurodegeneration. However, due to the cross-sectional design, causal inference is not possible, and reverse causation cannot be excluded. The modest effect size and reliance on self-reported dietary data necessitate cautious interpretation. These hypothesis-generating findings underscore the need for prospective cohort studies to confirm whether antioxidant-rich diets could serve as a primary prevention strategy for AD.</p><p><strong>Conclusion: </strong>This cross-sectional study found a negative linear association between CDAI and AD prevalence in US adults. These hypothesis-generating findings require confirmation in prospective cohort studies.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium-to-Potassium Ratio and Alzheimer's Disease: A Mendelian Randomization Study.","authors":"Haruka Yoshida, Takuro Inoue, Shigenori Suzuki, Yasutake Tomata","doi":"10.2174/0115672050472115260421093303","DOIUrl":"https://doi.org/10.2174/0115672050472115260421093303","url":null,"abstract":"<p><strong>Introduction: </strong>A higher urinary sodium-to-potassium (Na/K) ratio has been associated with increased risk of hypertension and cardiovascular diseases, which are known risk factors for Alzheimer's Disease (AD). Mendelian Randomization (MR), which uses genetic variants as instrumental variables to infer causality while reducing confounding and reverse causation, was applied to investigate whether the urinary Na/K ratio is causally associated with AD risk.</p><p><strong>Methods: </strong>A two-sample MR study was conducted using 31 single-nucleotide polymorphisms associated with urinary Na/K ratio as instrumental variables. The primary analysis employed Genome- Wide Association Study (GWAS) summary statistics for AD (n=85,934 individuals, including ADby- proxy). For sensitivity analysis, GWAS data specific to clinically diagnosed late-onset AD (n=21,982 individuals) were analyzed.</p><p><strong>Results: </strong>Genetically predicted urinary Na/K ratio was not statistically significantly associated with AD risk in the primary analysis; odds ratio (OR per 1 mol/mol increase) = 1.02, 95% confidence interval (CI): 0.77-1.36. In the sensitivity analysis using clinically diagnosed late-onset AD, the point estimate was higher (OR = 1.49, 95% CI: 0.99-2.24), although the association was not statistically significant.</p><p><strong>Discussion: </strong>Although no statistically significant causal association was observed, the study's findings may be consistent with previous observational studies linking higher sodium intake or a higher urine Na/K ratio to poorer cognitive performance. However, the sensitivity analysis suggested a possible association that warrants further investigation in larger MR studies using clinically confirmed AD datasets. As all data were derived from individuals of European ancestry, generalizability to other populations may be limited.</p><p><strong>Conclusion: </strong>This MR study did not provide clear evidence supporting a causal association between urinary Na/K ratio and AD risk.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voice Biomarkers: Cognitive Impairment, including Alzheimer's Disease, Dementia, or Mild Cognitive Impairment: Introduction to Peripheral Neuropathy.","authors":"Fatma Özcan","doi":"10.2174/0115672050454281260307134058","DOIUrl":"https://doi.org/10.2174/0115672050454281260307134058","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Alzheimer's disease (AD) can cause certain nervous disorders, which in turn can lead to voice disorders and abnormal values for certain acoustic parameters. Mild cognitive impairment (MCI) is probably the early stage of the disease. Dementia is one of the causes of Alzheimer's disease. Whether or not there is a link between these three cognitive impairments, lesions affecting the vocal cords or articulators can be caused by neurological structures that influence phonation. The potential of biomarkers in the detection of cognitive impairment is remarkable. In our study, we will examine vocal biomarkers obtained from the extraction of acoustic features. The aim of this study is to combine vocal biomarkers with cognitive diseases.</p><p><strong>Methods: </strong>The standardised dataset used has recently been made publicly available. Cognitive impairment, including Alzheimer's disease, dementia, or MCI, is diagnosed from /a/ and diadochokinesis-pataka vocalisations using Mel-Frequency Cepstral Coefficients (MFCCs) transformed into 2D scalogram images. For processing, we will use the pre-trained OpenL3 network, and our less resource-intensive network called Op1Net to classify diseased and healthy groups.</p><p><strong>Results: </strong>A significant difference was observed compared to the control group. For the /a/ vocalisation, classification accuracy across all ages and genders was 82.1%, and the AUC value was 88.3%, while for diadochokinesis-pataka, accuracy was 69.8% and the AUC value was 75.4%. In the group of women over 55 years of age, the accuracy was 80.93%, and the AUC value was 87.12%.</p><p><strong>Discussion: </strong>Performance results clearly show that there is a correlation between the voice and the neurodegenerative disease AD, dementia, or MCI. We can see that the results of the data classification, including all ages and genders, for the sound /a/ are higher than those for the 'pataka' vocalisations. The prolonged vowel provides more information about the disease.</p><p><strong>Conclusion: </strong>This preliminary multidisciplinary study clearly demonstrates the existence of a link between neurological disease and the voice, and raises several questions concerning the nervous system, particularly the vagus nerve and associated neuropathy.</p>","PeriodicalId":94309,"journal":{"name":"Current Alzheimer research","volume":" ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147629740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}