Journal of Alzheimer's disease reports最新文献

{"title":"Long-term safety and tolerability of brexpiprazole for Japanese patients with agitation in Alzheimer's disease dementia: A multicenter, open-label study.","authors":"Yu Nakamura, Jun Adachi, Naoki Hirota, Katsuhiro Iba, Koichi Shimizu, Masami Nakai, Naoki Mori, Kaneyoshi Takahashi","doi":"10.1177/25424823251334054","DOIUrl":"https://doi.org/10.1177/25424823251334054","url":null,"abstract":"<p><strong>Background: </strong>The long-term safety and efficacy of brexpiprazole in Asian patients with agitation associated with dementia due to Alzheimer's disease are unknown.</p><p><strong>Objectives: </strong>To evaluate the safety of 14-week treatment with brexpiprazole 1 or 2 mg/day in Japanese patients who completed the 10-week double-blind treatment period in a parent phase 2/3 study, and to explore the efficacy of brexpiprazole.</p><p><strong>Methods: </strong>This was a phase 3 multicenter, open-label study (ClinicalTrials.gov Identifier NCT03724942, registered on 28 October 2018). Patients who had completed 10-week treatment of placebo, 1 or 2 mg/day of brexpiprazole in a parent study were rolled over into this extended study. The primary endpoint was the frequency of adverse events.</p><p><strong>Results: </strong>Of 183 patients with informed consent, 164 were treated with brexpiprazole 1 or 2 mg/day for 14 weeks (prior brexpiprazole subgroup: 102 patients, prior placebo subgroup: 62 patients), and the overall study completion rate was 71.3%. The overall incidence of treatment-emergent adverse events was 90.2% (in each subgroup, 90.2% and 90.3%, respectively). Most treatment-emergent adverse events were mild or moderate in severity, and no new safety signals were observed. Regarding the Cohen-Mansfield Agitation Inventory total score at Week 14 (last observation carried forward), the mean change from baseline (standard deviation) was -4.0 (9.8).</p><p><strong>Conclusions: </strong>The extended 14-week treatment with brexpiprazole 1 or 2 mg/day after 10-week treatment was generally well tolerated in Japanese patients with agitation associated with dementia due to Alzheimer's disease, and the efficacy was maintained.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251334054"},"PeriodicalIF":2.8,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144054496","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 relationship of ¹⁸F-FDG-PET to other common biomarkers of dementia in a clinical cohort with memory deficits.","authors":"Katharina Woyk, Niels Hansen, Jens Wiltfang, Claudia Lange, Caroline Bouter","doi":"10.1177/25424823251314392","DOIUrl":"https://doi.org/10.1177/25424823251314392","url":null,"abstract":"<p><strong>Background: </strong>Early biomarker-based diagnosis of Alzheimer's disease (AD) is essential, particularly with the increasing availability of new therapeutic options. However, the relationship between imaging and cerebrospinal fluid (CSF) biomarkers, especially in the context of ¹⁸Fluorine-fluorodeoxyglucose positron emission tomography (¹⁸F-FDG-PET), remains insufficiently understood.</p><p><strong>Objective: </strong>The aim of this study was the evaluation of the relationship between ¹⁸F-FDG-PET and other common fluid and imaging AD-biomarkers in a clinical cohort of patients with cognitive decline and suspected AD.</p><p><strong>Methods: </strong>We included n = 90 patients with cognitive decline and clinically suspected AD that underwent ¹⁸F-FDG-PET imagining at our facility. Clinical and imaging data including patient characteristics, CSF biomarkers, Mini-Mental State Examination (MMSE), ¹⁸F-FDG-PET and ¹⁸F-Florbetaben-PET were retrospectively analyzed. PET images were quantified in several brain regions.</p><p><strong>Results: </strong>¹⁸F-FDG uptake correlated with CSF amyloid-β (Aβ)₄₀, Aβ₄₂, and the Aβ_42/40 ratio in several brain regions, but not with regional ¹⁸F-Florbetaben uptake. ¹⁸F-FDG uptake inversely correlated with t-tau and p-tau in CSF. Furthermore, a correlation between MMSE and ¹⁸F-FDG uptake was also detected in several brain regions. ¹⁸F-FDG-PET and its combination with CSF markers showed the highest predictive power for disease severity.</p><p><strong>Conclusions: </strong>The study highlights the potential of integrating ¹⁸F-FDG-PET with CSF biomarkers to improve the diagnosis, prognosis, and monitoring of AD, emphasizing the complexity and regional specificity of biomarker interactions in neurodegeneration.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251314392"},"PeriodicalIF":2.8,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144052277","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":"Sociodemographic and clinical profile from the Brazilian very old 90+ study (BRAVO-90+).","authors":"Aline Maria Macagnan Ciciliati, Renata Elaine Paraizo Leite, Lea T Grinberg, Carlos Augusto Pasqualucci, Vitor Ribeiro Paes, Alberto Fernando Oliveira Justo, Renata Eloah de Lucena Ferretti-Rebustini, Eduardo Ferrioli, Claudia Kimie Suemoto","doi":"10.1177/25424823251336247","DOIUrl":"https://doi.org/10.1177/25424823251336247","url":null,"abstract":"<p><strong>Background: </strong>Cognitive impairment and disability are frequent among the oldest-old population, particularly in low- and middle-income countries (LMIC), where this population is rapidly increasing. However, studies on people aged 90 or older are scarce in these settings. Here we analyze the characteristics of the Brazilian Very Old 90+ (BRAVO 90+) study, a population-based sample of 90+ older adults who died in Sao Paulo, Brazil.</p><p><strong>Objective: </strong>To describe clinical and functional characteristics and investigate factors associated with cognitive impairment in Brazilian adults 90 years or older.</p><p><strong>Methods: </strong>Data were collected at the time of death. Postmortem cognitive evaluation regarding cognitive abilities three months before death was performed using the Clinical Dementia Rating (CDR) scale. We investigated factors associated with cognitive impairment selected by a Lasso regression.</p><p><strong>Results: </strong>Among 409 participants (mean age = 94 ± 3 years; 72% women; 69% white; average education = 3.3 ± 3.6 years), hypertension, diabetes, and heart failure were prevalent. Most participants had disabilities. The leading causes of death verified by autopsy were pulmonary edema, pneumonia, and ischemic myocardial disease. Although 48% scored a CDR greater or equal to 1, only 51% had a previous dementia diagnosis. Sedentary behavior, osteoarthritis, and depression were associated with higher odds of cognitive impairment, while married status, greater body mass index, hypertension, and neoplasia were related to lower odds.</p><p><strong>Conclusions: </strong>Cognitive impairment and disability were common among Brazilians aged 90+. The BRAVO 90+ study will provide valuable insights into dementia and resilience in this population.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251336247"},"PeriodicalIF":2.8,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144055663","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":"Potential cure of Alzheimer's disease by reducing the level of Cdk5 using two drugs, each with a different modus operandi.","authors":"Jeffrey Fessel","doi":"10.1177/25424823251335870","DOIUrl":"https://doi.org/10.1177/25424823251335870","url":null,"abstract":"<p><p>There is need to understand the direct cause and, therefore, the appropriate treatment, of Alzheimer's disease (AD). A Google search was used to discern a) the primary cause of AD, and b) its treatment. Activation of Cdk5 is the primary cause for AD. Activation of Cdk5 may be decreased by using two drugs, roscovitine and tamoxifen, each having a different mechanism of action. Clinical trials should validate the efficacy and safety of using roscovitine and tamoxifen.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251335870"},"PeriodicalIF":2.8,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12033570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036281","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":"Cerebrospinal fluid Visinin-like protein-1 was associated with the relationship of body mass index with Alzheimer's disease pathology and cognition in non-demented elderly.","authors":"Yayu Wang, Siqi Yu, Man Zhang, Huaiyuan Zhu, Shujian Chen, Yajun Zhou, Xia Zhou, Zhongwu Sun, Xianfeng Yu, Xiaoqun Zhu","doi":"10.1177/25424823251331000","DOIUrl":"10.1177/25424823251331000","url":null,"abstract":"<p><strong>Background: </strong>The relationship and mechanisms between body mass index (BMI) and cognition are complex and inconclusive. Additionally, the role of neuronal calcium dysfunction, reflected by cerebrospinal fluid (CSF) Visinin-like protein 1 (VILIP-1), in the mechanisms linked with BMI and Alzheimer's disease (AD) has not been investigated.</p><p><strong>Objective: </strong>To investigate the relationship between CSF VILIP-1, BMI, and AD pathologies in non-demented elderly at early stages of AD.</p><p><strong>Methods: </strong>Baseline CSF AD core biomarkers (amyloid-β₄₂ [Aβ₄₂], phosphorylated tau [P-tau], and total tau [T-tau]) were measured for 1201 non-demented participants, selected from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, among whom 128 had measurements of CSF VILIP-1. Multivariate linear regression, causal mediation analyses, and linear mixed effects models were conducted to detect these associations.</p><p><strong>Results: </strong>The average age of participants was 72.6. CSF VILIP-1 was decreased in A+/TN- (A-positive/T- and N- negative) group and elevated in A-/TN + (A-negative/T- or N-positive) and A+/TN + groups, as compared with A-/TN- group. In total participants, BMI was negatively related to CSF P-tau, T-tau, P-tau/Aβ₄₂ and T-tau/Aβ₄₂. Noticeable associations were also presented between CSF VILIP-1 and AD core biomarkers, but not with Aβ₄₂ after stratification by A/T/N scheme. Furthermore, the influences of BMI on CSF tau pathology were mediated by CSF VILIP-1. Higher baseline CSF VILIP-1 correspond to faster longitudinal cognitive decline.</p><p><strong>Conclusions: </strong>Our findings indicated that CSF VILIP-1 changed dynamically and might be a key mediator in the associations between BMI and tau pathology, providing new insights into understanding the mechanisms underlying BMI-related cognitive deficits in non-demented elderly.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251331000"},"PeriodicalIF":2.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782273","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 novel <i>SORL1</i> mutation in a pedigree affected by early-onset Alzheimer's disease.","authors":"Veronica Redaelli, Martina Ricci, Angelo Del Sole, Marina Piccione, Sara Prioni, Giacomina Rossi","doi":"10.1177/25424823241296017","DOIUrl":"10.1177/25424823241296017","url":null,"abstract":"<p><p>Familial cases of Alzheimer's disease (AD) with autosomal dominant transmission and early onset have a prevalence around 1%. Since only a small fraction of them has a monogenic inheritance due to <i>APP, PSEN1</i>, and <i>PSEN2</i> genes, genetic studies are ongoing to unravel the missing heritability. By sequencing panels including multiple dementia-related genes, we identified a novel likely pathogenic mutation in <i>SORL1</i> in a pedigree including five members affected by AD. This loss of function mutation may lead to a reduction of SORL1 receptor, worsening amyloidogenic burden. As the contribution of <i>SORL1</i> mutations to heritability of AD is presently not well established, we think that it is very important to signal new familial (likely) pathogenic <i>SORL1</i> mutations in order to define the actual genetic involvement of <i>SORL1</i> in AD pathogenesis.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823241296017"},"PeriodicalIF":2.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11967206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782257","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":"Identifying Alzheimer's disease genes in apolipoprotein E^-/- mice brains with confirmed <i>Porphyromonas gingivalis</i> entry.","authors":"Sim K Singhrao, Claudia Consoli","doi":"10.1177/25424823251332874","DOIUrl":"10.1177/25424823251332874","url":null,"abstract":"<p><strong>Background: </strong>The apolipoprotein E allele ε4 is the most well-known predisposing genetic risk factor for Alzheimer's disease (AD).</p><p><strong>Objective: </strong>To identify AD genes in apolipoprotein E^-/- (ApoE^-/-) mice brains with confirmed entry of <i>Porphyromonas gingivalis</i>.</p><p><strong>Methods: </strong>TaqMan™ Mouse AD arrays were performed on orally infected ApoE^-/- mice with confirmed <i>P. gingivalis</i> entry and compared with sham infected mice brains (N = 4) at 12- and 24-weeks post infection.</p><p><strong>Results: </strong>Gene expression by qPCR demonstrated that in the <i>P. gingivalis</i> 12-weeks post oral infection, two genes were statistically significantly changed in their expression. These were cyclin dependent kinase 5 regulatory subunit 1 (Cdk5r1, 0.15 logfold change, p = 0.05) and Interleukin 1 alpha, (IL1a, -0.10 log fold change, p = 0.012). In the <i>P. gingivalis</i> 24-weeks post oral infection, three genes were statistically significantly changed in their expression. These were cholinergic receptor nicotinic alpha 7 subunit or Chrna7 (0.10 log fold change, p = 0.02), mitogen-activated protein kinase 1 or Mapk1 (0.10 log fold change, p = 0.05) and visinin like 1 or Vnsl1 (0.01 log fold change, p = 0.04). 87 out of 92 AD target genes demonstrated no difference between infected and sham mice brains.</p><p><strong>Conclusions: </strong>Five genes, from a recognized AD panel had statistically significantly altered expression in the ApoE^-/- mouse AD model following <i>P. gingivalis</i> entry into the brain. This suggests the ApoE^-/- genetic variation may control the biological activity of specific genes relevant to inflammation and neuronal plasticity following <i>P. gingivalis</i> infection.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251332874"},"PeriodicalIF":2.8,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11960171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766105","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":"Cerebrospinal fluid cytokine levels affect electroencephalographic activity in Alzheimer's disease.","authors":"Matilde Bruno, Chiara Giuseppina Bonomi, Alessandro Castelli, Francesca Izzi, Fabio Placidi, Silvia Falletti, Nicola Biagio Mercuri, Caterina Motta, Alessandro Martorana","doi":"10.1177/25424823241306772","DOIUrl":"10.1177/25424823241306772","url":null,"abstract":"<p><p>To investigate the role of neuroinflammation as mediator of amyloid-β-induced cortical activity changes in Alzheimer's disease (AD), we examined the relationship between cerebrospinal fluid (CSF) inflammatory cytokines (IL-1β, IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17, TNF-α, IFN-γ, GM-CSF, G-CSF, MIP-1α, MCP-1) and electroencephalographic (EEG) abnormalities in a cohort of biologically defined AD patients (n = 55, M:F = 19:36, median age 73, Mini-Mental State Examination ≥ 22). We retrieved a positive association between IL-4 CSF levels and EEG background activity frequency; IL-7, IL-8, and IL-12 CSF levels were positively associated with the presence of interictal epileptiform discharges. Neuroinflammation accompanying AD pathology may enhance the amyloid's epileptogenic potential while also counteracting neurodegenerative damage.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823241306772"},"PeriodicalIF":2.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756305","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 short-term impacts of COVID-2019 on depressive symptoms and cognitive decline: A community-based cohort study.","authors":"Mengmeng Ji, Darui Gao, Jie Liang, Yanyu Zhang, Yang Pan, Wenya Zhang, Yanjun Ma, Yongqian Wang, Chenglong Li, Yidan Zhu, Fanfan Zheng, Wuxiang Xie","doi":"10.1177/25424823251328627","DOIUrl":"10.1177/25424823251328627","url":null,"abstract":"<p><strong>Background: </strong>Neurological and psychological sequelae may persist after the infection of coronavirus disease 2019 (COVID-19). Depression and cognitive decline could increase the risk of Alzheimer's disease.</p><p><strong>Objective: </strong>To estimate the impacts of COVID-19 on depressive symptoms and cognitive decline.</p><p><strong>Methods: </strong>The data was from Beijing Research on Ageing and Vessel (BRAVE), which included all residents in the Xishan community. The first wave survey was performed from October to November 2019 (baseline) before the COVID-19 pandemic. The second wave survey was interrupted into two periods due to the introduction of the Ten New Measures, from October to November 2022 (no participants were infected) and from March to April 2023 (most participants were infected), providing an excellent opportunity to investigate the short-term impacts of COVID-19 on depressive symptoms and cognitive function with linear mixed models.</p><p><strong>Results: </strong>Among a total of 1012 participants, the median (interquartile range, IQR) age at baseline was 60.00 (56.00, 65.00) years, with 374 (36.96%) men and 479 participants COVID-19 infected. Compared with uninfected participants, the infected did not suffer pronounced depressive symptoms (β = -0.047; 95% CI -0.204 to 0.110) and accelerated declines in global cognition (β = 0.116; 95% CI -0.001 to 0.234) from wave 1 to wave 2. Sensitive analyses shared generally consistent findings.</p><p><strong>Conclusions: </strong>The impacts of COVID-19 infection on depressive symptoms and cognitive decline were not significant among participants in the BRAVE cohort. Further research is needed to investigate the long-term impacts on neurological and psychiatric symptoms.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251328627"},"PeriodicalIF":2.8,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11946293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733508","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":"Demographic predictors of cognitive performance in participants of a local substance abuse recovery program.","authors":"Ge Wang, Huijun Yi, Daniel Y Li, Elizabeth J Arnold, Damien C Bynum, Isaiah Chamoun, Jordie Johnson, Runze Ma, Shelby A Sliman, Wei Li","doi":"10.1177/25424823251328239","DOIUrl":"10.1177/25424823251328239","url":null,"abstract":"<p><strong>Background: </strong>Cognitive impairments have been reported among disadvantaged populations.</p><p><strong>Objective: </strong>We aimed to ascertain how demographic factors are associated with cognitive performance in individuals enrolled in a local substance abuse recovery program.</p><p><strong>Methods: </strong>In total, 106 participants were included in the study. Besides demographic information, vital signs and cognitive function, measured by Mini-Mental State Examination (MMSE) or Montreal Cognitive Assessment (MoCA), were collected from each participant. Welch's t-test and regression analysis were used to analyze how different demographic factors are associated with cognitive assessment scores.</p><p><strong>Results: </strong>The mean age of African American (AA) participants (n = 43) were 48.35 ± 1.65 years, which are older than that for the White participants of 38.95 ± 1.36 (n = 63) years. Compared to the AA participants, the White participants had a larger variance in attained education levels. The average MMSE scores were 27.09 ± 0.40 for AA participants, which is lower than that for the White participants of 28.52 ± 0.33 (<i>p </i>< 0.05). The average MoCA scores were 23.71 ± 0.54 for AAs, which is lower that for the White participants of 26.65 ± 0.44 (<i>p </i>< 0.001). The AA and White participant groups had cognitive impairment rate of 18.6% and 6.35%, respectively. The regression analysis indicates age and education are two significant predictors for the cognitive performance difference between the two racial groups.</p><p><strong>Conclusions: </strong>Significant disparities in cognitive performance exist between two racial groups of enrolled in a local substance abuse recovery program. The older age and lower levels of attained education in AA participants can explain the poorer cognitive function than the White participants.</p>","PeriodicalId":73594,"journal":{"name":"Journal of Alzheimer's disease reports","volume":"9 ","pages":"25424823251328239"},"PeriodicalIF":2.8,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143722745","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}