Journal of Alzheimer's disease reports最新文献

{"title":"Retinal thickness is associated with global cognition and executive function in mild cognitive impairment due to Alzheimer's disease.","authors":"Annahita Amireskandari, Camila Vieira Ligo Teixeira, Patrick Worhunsky, Cierra Keith, Joseph Malone, Melanie Ward, Marc W Haut, Tony Realini, Victor Finomore, Ali Rezai","doi":"10.1177/25424823261472085","DOIUrl":"10.1177/25424823261472085","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a neurodegenerative disease that leads to cognitive impairment and dementia, and retinal imaging is being explored as a biomarker. We examined the differences in retinal thickness by optical coherence tomography (OCT) between 47 participants with mild cognitive impairment due to Alzheimer's disease (Aβ+MCI) and 23 age-matched controls, as well as associations between cognition and OCT. There was no significant difference in retinal thickness between groups. However, retinal measures were robustly associated with global cognition and executive function in those with Aβ+MCI. Further studies with larger samples are needed to understand the clinical utility of OCT in AD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261472085"},"PeriodicalIF":2.8,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198416","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":"The evolutionary origins of dementia.","authors":"Jonathan Stone, Daniel M Johnstone, Rebecca S Mason, John Mitrofanis, Stephen R Robinson","doi":"10.1177/25424823261470053","DOIUrl":"https://doi.org/10.1177/25424823261470053","url":null,"abstract":"<p><p>Evidence has grown that the core pathology of age-related dementias, including Alzheimer's disease, is microvascular-small, symptomless bleeds from cerebral capillaries, accelerated by the hypertension of age. Each such bleed, this evidence suggests, damages a patch of brain, causing the death of neurons. This review asks how this vulnerability of the brain emerged from evolution, to cause age-related dementia? And has the vulnerability spurred the evolution of mitigating mechanisms? It is argued that seven features of human evolution contribute to the cause of dementia: the dependence of our tissues, especially the brain, on oxygen; the toxicity of the molecule (heme) that binds to oxygen to enable its transport; the pulsatility of the heart; the danger of glutamate as an excitatory neurotransmitter; the irreparability of elastin; the low level of adult neurogenesis in humans; and the breakdown, in late life, of the blood-brain barrier. Also discussed are mechanisms that have evolved to counter these threats to the brain, including the generation of a reserve of brain tissue. We argue that the vulnerabilities of the brain to damage that accumulates throughout life, and leads to dementia in the aged, were established early in the evolution of vertebrates. Several can be understood as unavoidable yet damaging outcomes of highly advantageous steps in evolution. Human cognition fails when and because, with age, the damage that results from these vulnerabilities overwhelms the evolved protections and exhausts any reserve of brain tissue. Implications of these vulnerabilities for the delay and management of dementia are discussed.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261470053"},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149119802","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":"Association between Gompertz law-based biological age (GOLD BioAge) and incident mild cognitive impairment: Modifying role of social activeness.","authors":"Yating Xiao, Li Li","doi":"10.1177/25424823261470071","DOIUrl":"10.1177/25424823261470071","url":null,"abstract":"<p><strong>Background: </strong>Mild cognitive impairment (MCI) is an important transitional stage between normal cognitive aging and dementia. Biomarker-based biological age may better capture physiological aging processes than chronological age, yet its association with the risk of developing MCI remains insufficiently studied.</p><p><strong>Objective: </strong>We aimed to examine the association between Gompertz Law-Based Biological Age (Light BioAge) and incident MCI in a middle-aged and older Chinese population, and to explore whether social activeness modifies this association.</p><p><strong>Methods: </strong>We used data from the China Health and Retirement Longitudinal Study, a nationally representative cohort. Light BioAge was calculated from chronological age, serum creatinine, fasting glucose, and C-reactive protein. Incident MCI was defined using age- and education-standardized cognitive assessments. Cox regressions were used to analysis.</p><p><strong>Results: </strong>Among 9410 participants free of MCI at baseline, 1047 developed MCI during follow-up. Light BioAge was negatively associated with risk of MCI (hazards ratio (HR) = 0.99, 95% CI: 0.98-0.99). Compared to high Light BioAge, those in the moderate and low groups showed significantly lower risks of MCI (HR = 0.78, 95% CI: 0.65-0.94 and HR = 0.79, 95% CI: 0.65-0.97, respectively). The association were consistent across sex and different levels of social activeness, with no significant interaction observed.</p><p><strong>Conclusions: </strong>Lower biological age, as estimated by Light BioAge, is independently associated with a reduced risk of MCI in middle-aged and older adults. The use of biomarker-based aging indicators may help identify individuals at higher risk of cognitive decline for early preventive strategies.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261470071"},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186814","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":"Machine learning-based screening for Ascertain Dementia 8-defined suspected cognitive impairment leveraging routine health check data in South China.","authors":"Peiyue Su, Jiale Li, Yang Hu, Yue Xu, Qianqian Ji, Qi Liu, Xiaoping Huang, Ruitong Liao, Liuqing Li, Yueting Liao, Yunzhang Wang, Yifan Lin, Yiqiang Zhan","doi":"10.1177/25424823261470033","DOIUrl":"10.1177/25424823261470033","url":null,"abstract":"<p><strong>Background: </strong>Timely detection of cognitive concerns can facilitate further assessment, referral, and management; however, cognitive impairment often remains under-detected in primary care settings, representing a missed opportunity for early detection for Alzheimer's disease and related dementias.</p><p><strong>Objective: </strong>We aimed to develop and internally validate a machine learning-based cross-sectional concurrent classification model that utilizes routine health check data only, supporting concurrent identification of individuals with Ascertain Dementia 8 (AD8)-defined suspected cognitive impairment who warrant further clinical cognitive evaluation.</p><p><strong>Methods: </strong>This cross-sectional study included 7440 adults (aged ≥65 years) from the 2021 Elderly Health Check Program in Shenzhen, China. Suspected cognitive impairment was defined as an AD8 score ≥2. Following data splitting, feature selection was processed via the Boruta algorithm. Five algorithms-logistic regression, random forest, XGBoost, SVM, and EasyEnsemble-were evaluated. Performance was assessed using ROC, PR, accuracy, sensitivity, specificity, PPV, NPV, NNS, DCA, calibration plots, and Brier score.</p><p><strong>Results: </strong>The EasyEnsemble model outperformed other algorithms on the independent testing set, with an ROC-AUC of 0.696 (Bootstrap-corrected mean: 0.677; 95% CI: 0.643-0.713). At the clinically optimized threshold of 0.034, the model achieved a sensitivity of 60.6%, a specificity of 73.4% and a NNS of 51.9. DCA indicated a positive net benefit across a threshold range approximately from 0.03 to 0.20, suggesting potential clinical utility for triage in this setting.</p><p><strong>Conclusions: </strong>This cross-sectional model provides a pragmatic, low-cost tool for concurrent case-finding of individuals with AD8-defined suspected cognitive impairment in primary care. However, further external validation in diverse geographic regions is mandatory before clinical implementation.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261470033"},"PeriodicalIF":2.8,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186394","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":"Frequent pain moderates the association between brain-derived neurotrophic factor and plasma Alzheimer's disease biomarkers in early midlife.","authors":"Tyler R Bell, Brianna N Lockwood, Kayleigh N Muniz, Lydia C Kang, Makenzie N Laughery, Sophia S Stowell, Sana M Bham, Rongxiang Tang","doi":"10.1177/25424823261470037","DOIUrl":"10.1177/25424823261470037","url":null,"abstract":"<p><p>Brain-derived neurotrophic factor (BDNF) is a neurotrophin regulating neuroplasticity and is reduced in Alzheimer's disease (AD). Whether BDNF relates to AD pathophysiology in dementia-free individuals and under what conditions remain unknown. Pain, a prevalent midlife condition and AD risk factor, engages BDNF signaling. We examined whether frequent pain moderated associations between BDNF and AD plasma biomarkers (ptau217, BD-tau) in early midlife (Mean age=45.8). Among individuals with frequent pain, higher BDNF was associated with lower BD-tau and ptau217. No associations emerged among pain-free individuals. These findings suggest BDNF-indexed neuroplasticity may buffer against AD pathology and neurodegeneration in the context of pain.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261470037"},"PeriodicalIF":2.8,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198312","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":"Psychometric evaluation of the Turkish version of the Bangor Dementia Resilience Scale.","authors":"Burcu Akpınar Söylemez, Merve Aliye Akyol, Ecem Özgül, Hasret Erden, Özlem Küçükgüçlü, Marianna Tsatali, Görsev Yener, Birgit Teichmann","doi":"10.1177/25424823261461527","DOIUrl":"https://doi.org/10.1177/25424823261461527","url":null,"abstract":"<p><strong>Background: </strong>Resilience is an important positive construct supporting people with dementia; however, validated self-report instruments for this population remain limited, and no Turkish version is currently available.</p><p><strong>Objective: </strong>This study aimed to adapt the Bangor Dementia Resilience Scale (BDRS) into Turkish and to evaluate its psychometric properties in individuals with mild cognitive impairment (MCI) and early-stage dementia.</p><p><strong>Methods: </strong>This cross-sectional psychometric study included 118 individuals with MCI or early-stage dementia. The translation and cultural adaptation process followed established guidelines. Structural validity was examined using exploratory factor analysis (EFA). Convergent validity was assessed using Pearson correlations between the Turkish version of the BDRS (T-BDRS) scores and quality of life (QoL-AD), as well as clinical variables including Mini-Mental State Examination, Neuropsychiatric Inventory, and Katz Activities of Daily Living. Reliability was evaluated using Cronbach's alpha, McDonald's omega, item-total correlations, and test-retest reliability (n = 30).</p><p><strong>Results: </strong>EFA supported a five-factor structure explaining 68.32% of the total variance. The internal consistency of the total scale was excellent (Cronbach's α = 0.946; ω = 0.946). Item-total correlations ranged from 0.604 to 0.787. Test-retest reliability demonstrated excellent stability (ICC = 0.993). Convergent validity was supported by a strong positive correlation with QoL-AD (r = 0.819, 95% CI: 0.744-0.872, p < 0.001).</p><p><strong>Conclusions: </strong>The T-BDRS demonstrated satisfactory validity and reliability for assessing resilience in individuals with MCI and early-stage dementia. It represents a promising tool for research and clinical practice, supporting the assessment of positive psychosocial outcomes in dementia care.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261461527"},"PeriodicalIF":2.8,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662366/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198456","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":"Brain transcriptome-wide association study reveals selective long-term potentiation enrichment and negative directional skew of senescence-regulation pathways in Alzheimer's disease.","authors":"Ngo Cheung","doi":"10.1177/25424823261468711","DOIUrl":"https://doi.org/10.1177/25424823261468711","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) has a strong genetic component, but many risk loci are non-coding, limiting biological interpretation. Transcriptome-wide association studies (TWAS) help address this by imputing genetically regulated gene expression from genome-wide association study (GWAS) data.</p><p><strong>Objective: </strong>To test whether AD-associated genetically regulated brain expression is enriched in pathways related to synaptic plasticity, glial-immune biology, senescence, mitochondrial function, nicotinamide adenine dinucleotide (NAD) metabolism, and metabolic signaling.</p><p><strong>Methods: </strong>We applied S-PrediXcan to the European-ancestry AD GWAS meta-analysis from Bellenguez et al. (2022) across six brain tissues. Tissue-specific results were combined using Stouffer meta-analysis. Approximately 40 curated gene sets from public pathway databases and adult brain cell-type signatures were tested. Enrichment was assessed using Stouffer z-scores, Wilcoxon tests, and permutation p-values. Sensitivity analyses examined tissue consistency, top-driver removal, gene-level Z thresholds, gene-set overlap, and MHC/immune-gene exclusion.</p><p><strong>Results: </strong>The strongest positive enrichment was long-term potentiation (LTP), particularly KEGG LTP ALL, with a Stouffer z-score of +5.267. Astrocyte-expressed genes were positively enriched and exceeded microglial signatures. Complement enrichment was largely driven by CR1, while synapse pruning was negatively enriched. Insulin, GLP-1, and PI3K-AKT-mTOR pathways also showed positive enrichment. Senescence regulation and oxidative phosphorylation showed the strongest negative skews. NAD-related sets showed mixed gene-specific effects. Sensitivity analyses identified senescence regulation, LTP, oxidative phosphorylation, and PI3K-AKT-mTOR as the most robust signals.</p><p><strong>Conclusions: </strong>AD genetic liability captured by brain TWAS converges on glial-immune signaling, selective synaptic potentiation, and metabolic pathways, while senescence regulation and oxidative phosphorylation show directional depletion. These findings support pathway-based stratification to guide precision therapeutic approaches in AD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261468711"},"PeriodicalIF":2.8,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662292/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198126","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":"Smaller pineal volume in Alzheimer's disease than in dementia with Lewy bodies.","authors":"Teruyuki Matsuoka, Ryota Kobayashi, Ayu Imai, Kazutaka Sakamoto, Daichi Morioka, Akihito Suzuki, Noriyuki Kimura, Teruaki Masuda, Takuya Ataka, Jin Narumoto","doi":"10.1177/25424823261468305","DOIUrl":"10.1177/25424823261468305","url":null,"abstract":"<p><strong>Background: </strong>Pineal gland volume reduction in Alzheimer's disease (AD) has been reported. Recent findings also indicate an association between pineal volume reduction and dementia with Lewy bodies (DLB).</p><p><strong>Objective: </strong>This study aimed to compare pineal volume between two major neurodegenerative disorders: AD and DLB.</p><p><strong>Methods: </strong>This cross-sectional analysis included patients with AD or DLB who underwent brain magnetic resonance imaging (MRI) and Mini-Mental State Examination (MMSE). AD was diagnosed based on the National Institute on Aging-Alzheimer's Association criteria and confirmed by positive amyloid positron emission tomography. DLB was diagnosed per McKeith et al.'s clinical criteria and confirmed by dopamine transporter single-photon emission computed tomography or ¹²³I-metaiodobenzylguanidine myocardial scintigraphy. Pineal parenchymal volume (PPV) was manually measured using MRI data. The Mann-Whitney U test was used for group comparisons, and analysis of covariance (ANCOVA) was performed with logarithmic transformation since PPV was not normally distributed. Covariates included total intracranial volume, age, sex, MMSE score, use of antidementia drugs, use of psychotropic medications, and MRI magnetic field strength.</p><p><strong>Results: </strong>Seventy-five patients (AD, 41; DLB, 34; 35 women) were analyzed. PPV was significantly smaller in the AD group than in the DLB group (74.7 ± 18.8 versus 96.0 ± 31.6 mm³, U = 1024, p < 0.001). ANCOVA confirmed a significant diagnostic effect (F = 11.9, p < 0.001).</p><p><strong>Conclusions: </strong>Pineal volume was smaller in AD than in DLB; this difference may reflect the neuropathological characteristics specific to AD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261468305"},"PeriodicalIF":2.8,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186616","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":"Development and prospect of treating Alzheimer's disease using the glymphatic system.","authors":"Jiajie Gu, Zekai Liu, Jiaxiang Gu","doi":"10.1177/25424823261461528","DOIUrl":"10.1177/25424823261461528","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a common neurodegenerative disorder with progressive cognitive decline and typical amyloid-β (Aβ) and tau pathologies, whose pathogenesis remains unclear. The glymphatic system, a core cerebral waste clearance pathway, has become a critical target for AD pathogenic research and novel therapy development. This review explores the glymphatic system's structure and function, illustrates its correlation with AD pathogenesis, summarizes targeted therapies, and highlights research limitations and future directions to facilitate AD translational research. Relevant literatures published from 2012 to 2025 were retrieved from PubMed and Web of Science databases with the combined keywords of \"Alzheimer's disease\", \"glymphatic system\", \"meningeal lymphatic vessels\", \"Aβ clearance\" and \"lymphatic therapy for AD\". The included literatures were systematically sorted, and the basic mechanism, therapeutic strategy and research limitations were analyzed and summarized. The glymphatic system clears 30%-50% of cerebral Aβ in rodent models via meningeal lymphatic and parenchymal pathways, yet human evidence is lacking. Glymphatic dysfunction, <i>APOE4</i> genotype, and immune imbalance promote Aβ and tau accumulation and AD progression. Several glymphatic-targeted strategies have demonstrated preclinical efficacy, with intranasal agents and photostimulation progressing into early-phase clinical trials. The glymphatic system is a promising therapeutic target for AD by improving brain waste clearance. Existing limitations include species discrepancies, unclear causal relationships and insufficient clinical data. Future research will focus on human-specific mechanisms, staged intervention strategies, and rigorous safety evaluation of targeted treatments.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261461528"},"PeriodicalIF":2.8,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186746","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":"Screening of herbs for vascular dementia: Through the combination of reverse network pharmacology and traditional Chinese medicine enrichment analysis.","authors":"Xiaokui Yuan, Qin Tang, Tong Wang","doi":"10.1177/25424823261466619","DOIUrl":"https://doi.org/10.1177/25424823261466619","url":null,"abstract":"<p><strong>Background: </strong>Vascular dementia (VaD) represents the second most prevalent form of cognitive impairment following Alzheimer's disease. Its pathological mechanisms encompass a complex interplay of cerebral ischemia, inflammatory responses, oxidative stress, and neuronal apoptosis. Current clinical interventions predominantly target cerebral circulation enhancement and neuroprotection; however, these approaches exhibit limitations in efficacy, single-target specificity, and significant adverse effects. Traditional Chinese medicine (TCM) offers a novel therapeutic paradigm for complex diseases owing to its multi-target synergistic effects, low toxicity profile, and integrated preventive and therapeutic benefits.</p><p><strong>Objective: </strong>This study aims to identify the potentially effective active components in TCM targeting VaD, and to elucidate the multi-target regulatory mechanisms.</p><p><strong>Methods: </strong>This study employed a \"disease-gene-drug\" reverse screening model, integrating bioinformatics and network pharmacology, to systematically identify potential TCM candidates for VaD treatment and elucidate their multi-target regulatory mechanisms.</p><p><strong>Results: </strong>A total of eight TCM agents with potential VaD therapeutic efficacy (including Niuxi, Pueraria lobata, and Citrus aurantium) were identified, alongside nine active compounds and nine therapeutic targets. Notably, Gehua and Zhike were reported for the first time to exhibit potential VaD therapeutic effects. Furthermore, molecular docking technology was utilized to investigate the binding affinity and interaction modes of these nine active compounds with key targets.</p><p><strong>Conclusions: </strong>To our knowledge, this study is among the first to apply reverse network pharmacology combined with TCM enrichment specifically to VaD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"10 ","pages":"25424823261466619"},"PeriodicalIF":2.8,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149198465","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}