Journal of Alzheimer's disease reports最新文献

{"title":"Feasibility of expiratory muscle strength training to address oropharyngeal dysphagia in a patient living with mixed dementia: A case report.","authors":"Joanne Yee, Sara Gustafson, Raele Donetha Loy, Nicole Rogus-Pulia","doi":"10.1177/25424823251361032","DOIUrl":"10.1177/25424823251361032","url":null,"abstract":"<p><p>Oropharyngeal dysphagia frequently occurs in persons living with Alzheimer's disease and related dementias (PLWD) and results in negative health consequences. Strength-based exercises may address swallowing biomechanical impairments. Expiratory muscle strength training (EMST) is an intervention examined in other neurodegenerative populations and has demonstrated promise for improving respiratory muscle strength and airway defense physiologic capacity, potentially improving swallowing safety. We describe a case of a patient with Alzheimer's disease who participated in five consecutive weeks of EMST. We demonstrate that EMST is a feasible intervention for PLWD. Further research should be conducted to assess efficacy and benefit of EMST for PLWD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251361032"},"PeriodicalIF":2.8,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981262","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 preventive role of tempeh isoflavones on menopausal women's cognitive function: A multiple mechanism pathway.","authors":"Atik Kridawati, Lili Indrawati, Sugeng Hadisaputra, Asyifa Robiatul Adawiyah","doi":"10.1177/25424823251371284","DOIUrl":"10.1177/25424823251371284","url":null,"abstract":"<p><p>Cognitive dysfunction in the elderly is not only a disease but also could be considered a preclinical condition of Alzheimer's disease (AD), one of the most common types of dementia in the elderly. Therefore, treatment such as early detection and management of risk factors that could slow and prevent the onset of dementia is necessary for the elderly. Estrogen reduces the risk of AD in postmenopausal women. It has also been shown to reduce amyloid-β (Aβ) pathology in animal models of AD and suppress Aβ secretion from neuronal tissue<i>.</i> Estrogen receptors are involved in cognitive processes such as learning and memory, the formation of the hippocampus, the amygdala, and the cerebral cortex. Hormone replacement therapy (HRT) could improve cognition and thus delay the development of AD. Giving HRT after 9 years has been shown to increase the risk of breast cancer two-fold and cardiovascular disease. Phytoestrogens are hormones found in plants that can be an alternative to HRT. One of the foods that contains phytoestrogens and is widely consumed in Indonesia is tempeh. Isoflavone is a dominant phytoestrogen, structurally an estrogen-like substance, and functionally similar to 17β-estradiol. In this review article, we will discuss the role of tempeh isoflavones in a mechanism pathway on cognition.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251371284"},"PeriodicalIF":2.8,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981290","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":"Longitudinal impact of cholinesterase inhibitors on cholinergic white matter integrity in mild cognitive impairment: A diffusion MRI study.","authors":"Elham Ramezannezhad","doi":"10.1177/25424823251374681","DOIUrl":"10.1177/25424823251374681","url":null,"abstract":"<p><strong>Background: </strong>Early degeneration of the cholinergic nucleus basalis of Meynert contributes to cognitive decline in Alzheimer's disease (AD). Microstructural damage in downstream cholinergic tracts-the cingulum bundle (CGC), entorhinal cortex (EC), and uncinate fasciculus (UNC)-often precedes volumetric atrophy. While cholinesterase inhibitors (ChEIs) can preserve cortical and hippocampal volume, their influence on white-matter integrity is unclear.</p><p><strong>Objective: </strong>To determine whether ChEIs slow microstructural decline in four cholinergic tracts (CGC, EC, UNC, posterior thalamic radiation [PTR]) in mild cognitive impairment (MCI), and whether baseline cognitive status modulates this effect.</p><p><strong>Methods: </strong>Diffusion-tensor imaging from the Alzheimer's Disease Neuroimaging Initiative was analyzed in 46 MCI participants receiving donepezil or rivastigmine and 62 untreated MCI controls, each scanned serially over two years. Fractional anisotropy (FA) and mean diffusivity (MD) indexed tract integrity. Linear mixed-effects models tested time × medication × baseline cognition (ADAS-Cog13) interactions, adjusting for age, sex, <i>APOE</i> ε4, and white-matter hyperintensity burden.</p><p><strong>Results: </strong>Across groups, CGC showed progressive degeneration (FA↓, MD↑; <i>p</i> < 0.001). Significant three-way interactions emerged for MD in bilateral CGC, FA in right EC, and MD in left PTR (all <i>p</i> < 0.01). ChEI users with milder baseline impairment (lower ADAS-Cog13) exhibited attenuated FA loss and MD increase, indicating slower microstructural decline; those with greater initial impairment derived minimal benefit. No medication effect was detected in UNC.</p><p><strong>Conclusions: </strong>ChEIs confer tract-specific, stage-dependent protection of cholinergic white matter, particularly in early MCI. The findings underscore the value of initiating ChEI therapy before substantial cognitive deterioration and highlight the need for stage-tailored interventions aimed at preserving white-matter integrity in prodromal AD.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251374681"},"PeriodicalIF":2.8,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981299","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 of cardiovascular disease with dementia: A longitudinal analysis using National Alzheimer's Coordinating Center data.","authors":"Diana Summanwar, Hyena Kim, Jingkai Wei, Malaz Boustani, Alvaro Alonso, Ambar Kulshreshtha","doi":"10.1177/25424823251370646","DOIUrl":"10.1177/25424823251370646","url":null,"abstract":"<p><p>We analyzed how cardiovascular disease subtypes influence the prevalence and incidence of dementia among 30,582 individuals aged 50 and older in the National Alzheimer's Coordinating Center cohort. We calculated prevalence ratios (aPR) and hazard ratios (aHR), using models adjusted for age, sex, race, years of education, hypertension, diabetes, and dyslipidemia. Stroke (aPR: 1.26; 95% CI: 1.20-1.32) and history of arrhythmias (aPR: 1.17; 95% CI: 1.09-1.24) were associated with higher dementia prevalence. In survival analysis, stroke was associated with a 55% increased risk of incident dementia (aHR: 1.55; 95% CI: 1.36-1.77).</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251370646"},"PeriodicalIF":2.8,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12371225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981272","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 mild cognitive impairment window for optimal Alzheimer's disease intervention.","authors":"Kevin Mekulu, Faisal Aqlan, Hui Yang","doi":"10.1177/25424823251370768","DOIUrl":"10.1177/25424823251370768","url":null,"abstract":"<p><p>The FDA approval of disease-modifying Alzheimer's disease therapies marks a major shift in treatment but exposes a critical challenge: identifying patients during the mild cognitive impairment (MCI) stage when intervention is most effective. Despite early biological changes, most diagnoses occur after significant decline. Drawing from over 180 stakeholder interviews conducted through the NSF I-Corps program reveal major detection gaps across primary care, specialty access, and available tools. This commentary highlights the consequences of delayed diagnosis and proposes translational strategies to align early detection with therapeutic opportunity, positioning MCI as the critical window for Alzheimer's disease intervention.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251370768"},"PeriodicalIF":2.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981304","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":"Probable lecanemab-associated pontine hemorrhage following cardiovascular intervention: Clinical implications for lecanemab use.","authors":"Siwei Chen, Yongan Sun, Lanqiu Yao, Qing Peng","doi":"10.1177/25424823251366998","DOIUrl":"10.1177/25424823251366998","url":null,"abstract":"<p><p>We report a 76-year-old patient with mild cognitive impairment and <i>APOE</i> ε3/ε3 genotype who developed a rare pontine hemorrhage following treatment with lecanemab, an anti-amyloid-β monoclonal antibody for Alzheimer's disease. She was initially on clopidogrel and rivaroxaban; rivaroxaban was discontinued prior to lecanemab initiation. After two infusions, lecanemab was paused due to angina. She then underwent coronary stenting and was placed on dual antiplatelet therapy (aspirin and clopidogrel). Pontine hemorrhage occurred after twenty days. This case highlights heightened bleeding risk when lecanemab is combined with intensified antithrombotic therapy, even without <i>APOE</i> ε4 or significant cerebral small vessel disease load.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251366998"},"PeriodicalIF":2.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981343","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":"Digital adaptation of odor identification test: Current knowledge, gaps, and initial insights from a DAC global cohort.","authors":"Jaishree Singh, Sara A Moustafa, Subhanjan Mondal, Farooq Waheed, Irene B Meier, Vaibhav A Narayan, Mie Rizig, Mohamed Salama","doi":"10.1177/25424823251362132","DOIUrl":"10.1177/25424823251362132","url":null,"abstract":"<p><strong>Background: </strong>Olfaction has enabled humans to survive and reproduce throughout their evolutionary history. Certain odors have been historically associated with danger while others, pleasure. Further, olfactory impairment is one of the earliest manifestations of neurodegeneration, such as Alzheimer's disease. Therefore, olfactory tests have the potential to reveal insights into a person's brain health. The landscape of orthonasal olfactory tools is vast, and many have been adapted for populations living in low- and middle-income countries, but challenges remain in the awareness of the utility of olfactory testing, effective deployment, and scalability.</p><p><strong>Objective: </strong>This report explores the current landscape of olfactory tests, the potential for digital tests to provide scalable data in low-resource settings, and their potential applicability in the Alzheimer's disease and brain health space. We also describe the ScentAware digital odor identification test and present some preliminary findings from its use in Egypt, a site for the Davos Alzheimer's Collaborative's Global Cohorts Program.</p><p><strong>Methods: </strong>The American University in Cairo in partnership with University College London collected olfactory data using the ScentAware test from 125 participants from the North African Dementia Registry, a longitudinal study of community dwelling adults over age 55 in Egypt and the surrounding Middle East and North Africa region.</p><p><strong>Results: </strong>Participants' olfactory function measured by the culturally adapted ScentAware test somewhat correlated with language and memory, as assessed by the Egyptian Harmonized Cognitive Assessment Protocol battery.</p><p><strong>Conclusions: </strong>Our adaptation of the ScentAware test suggests that digital olfactory assessment holds promise for cost-effective deployment at scale in a low-resource setting.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251362132"},"PeriodicalIF":2.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981266","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":"Inactivation of BACE2 stimulates release of endothelin-1 from human brain microvascular endothelial cells.","authors":"Tongrong He, Zvonimir S Katusic","doi":"10.1177/25424823251371040","DOIUrl":"10.1177/25424823251371040","url":null,"abstract":"<p><p>Beta-site amyloid precursor protein cleaving enzyme 2 (BACE2) is one of the most downregulated genes in the brain capillary endothelial cells derived from patients with Alzheimer's disease (AD). Endothelin-1 (ET-1) significantly contributes to the pathogenesis of AD. We hypothesized that loss of BACE2 increases production of ET-1 from human brain microvascular endothelial cells (BMECs). Genetic inactivation of BACE2 in cultured human BMECs significantly upregulated expression and release of ET-1. Mechanistic studies indicated that γ-aminobutyric acid type B receptor subunit 2/transforming growth factor beta 2 signaling pathway mediated the effect of BACE2 inhibition on ET-1 production.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251371040"},"PeriodicalIF":2.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12365451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981323","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":"Bibliometric analysis of pathological mechanisms in Alzheimer's disease: Applications based on mouse models.","authors":"Jinjiang Li, Zhaoxiong Lin, Yufei Niu, Wenrui Chang, Siyun Song, Guang Yang, Feng Liu, Jiaxin Dai, Chunyan Hao","doi":"10.1177/25424823251367046","DOIUrl":"10.1177/25424823251367046","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by memory loss and cognitive decline. Animal models play a key role in exploring its pathophysiological mechanisms.</p><p><strong>Objective: </strong>To analyze global research trends and knowledge structure in AD pathophysiological mechanisms based on animal models.</p><p><strong>Methods: </strong>Publications from 2014 to 2023 were retrieved from the Web of Science Core Collection. CiteSpace and VOSviewer were used for bibliometric analysis and data visualization.</p><p><strong>Results: </strong>A total of 2169 publications were identified, with a steady growth trend. The United States and China were the leading contributors, with Harvard University as a major collaborative hub. The Journal of Alzheimer's Disease published the most articles, while the Journal of Neuroscience had the highest co-citation frequency. Holtzman DM was a key author in the field. Nine keyword clusters were identified, including insulin resistance, amyloid beta, and oxidative stress. Emerging topics include synapse loss, gut microbiota, and NLRP3 inflammasome.</p><p><strong>Conclusions: </strong>This study provides a concise overview of global research on AD pathophysiological mechanisms in animal models, offering valuable insights for future research directions.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251367046"},"PeriodicalIF":2.8,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351105/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877150","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 bibliometric and systematic review of the global impact of air pollution on Alzheimer's disease: Insights from cohort studies.","authors":"Faezeh Jahedi, Gholamreza Goudarzi, Mehdi Ahmadi, Farhad Safdari","doi":"10.1177/25424823251368883","DOIUrl":"10.1177/25424823251368883","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence highlights the potential role of environmental factors, particularly air pollution, in the development and progression of Alzheimer's disease (AD). Air pollutants may contribute to neurodegenerative processes through mechanisms such as oxidative stress, neuroinflammation, and disruption of the blood-brain barrier.</p><p><strong>Objective: </strong>This review aims to systematically evaluate global cohort studies investigating the association between long-term exposure to key air pollutants-specifically particulate matter (PM2.5), nitrogen dioxide (NO₂), and ozone (O₃)-and the risk of AD.</p><p><strong>Methods: </strong>A total of 31 peer-reviewed cohort studies were included based on a structured search strategy. We analyzed epidemiological outcomes, exposure assessment methodologies, and geographic trends. Additionally, a bibliometric analysis was conducted using VOSviewer to identify major contributors and emerging research themes.</p><p><strong>Results: </strong>Findings indicate a consistent association between PM2.5 exposure and increased risk of AD, independent of genetic predisposition and lifestyle factors. Proposed biological mechanisms include oxidative stress, microglial activation, blood-brain barrier disruption, and amyloid-β accumulation. Bibliometric mapping revealed regional concentration of research in North America, Europe, and East Asia, with increasing global interest over the past decade.</p><p><strong>Conclusions: </strong>There is mounting evidence linking air pollution to Alzheimer's disease. Advances in exposure assessment have improved the accuracy of epidemiological findings. Public health policies targeting air quality control and further studies on molecular and early-life exposures are essential to mitigate the neurotoxic effects of environmental pollutants.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251368883"},"PeriodicalIF":2.8,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877149","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}