Alzheimer's Research & Therapy最新文献

{"title":"Differential effects of aging, Alzheimer's pathology, and APOE4 on longitudinal functional connectivity and episodic memory in older adults.","authors":"Larissa Fischer, Jenna N Adams, Eóin N Molloy, Niklas Vockert, Jennifer Tremblay-Mercier, Jordana Remz, Alexa Pichet Binette, Sylvia Villeneuve, Anne Maass","doi":"10.1186/s13195-025-01742-6","DOIUrl":"https://doi.org/10.1186/s13195-025-01742-6","url":null,"abstract":"<p><strong>Background: </strong>Both aging and Alzheimer's disease (AD) affect brain networks, with early disruptions occurring in regions involved in episodic memory. Few studies have, however, focused on distinguishing region-specific effects of AD-biomarker negative \"normal\" aging and early amyloid- and tau pathology on functional connectivity. Further, longitudinal studies combining imaging, biomarkers, and cognition are rare.</p><p><strong>Methods: </strong>We assessed resting-state functional connectivity (rsFC) strength and graph measures in the episodic memory network including the medial temporal lobe (MTL), posteromedial cortex (PMC), and medial prefrontal cortex alongside cognition over two years. For this preregistered study, we included 100 older adults who were amyloid- and tau-negative using CSF and PET measurements to investigate \"normal\" aging, and 70 older adults who had longitudinal CSF data available to investigate functional changes related to early AD pathology. All participants were cognitively unimpaired older adults from the PREVENT-AD cohort. We used region of interest (ROI)-to-ROI bivariate correlations, graph analysis, and multiple regression models.</p><p><strong>Results: </strong>In the amyloid- and tau-negative sample, rsFC strength within PMC, between parahippocampal cortex and inferomedial precuneus, and between posterior hippocampus and inferomedial precuneus decreased over time. Additionally, we observed a longitudinal decrease in global efficiency. Further, there was a steeper longitudinal decrease in rsFC and global efficiency with higher baseline age particularly of parahippocampal-gyrus regions. Further, lower rsFC strength within PMC was associated with poorer longitudinal episodic memory performance. In the sample with available CSF data, a steeper increase in rsFC between anterior hippocampus and superior precuneus was related to higher baseline AD pathology. Higher MTL-PMC rsFC strength was differentially associated with episodic memory trajectories depending on APOE4 genotype.</p><p><strong>Conclusions: </strong>Our findings suggest differential effects of aging and AD pathology. Hypoconnectivity within PMC was related to aging and cognitive decline. MTL-PMC hyperconnectivity was related to early AD pathology and cognitive decline in APOE4 carriers. Future studies should investigate more diverse samples, nonetheless, our approach allowed us to identify longitudinal functional changes related to aging and early AD pathology, enhancing cross-sectional research. Hyperconnectivity has been proposed as a mechanism related to early AD pathology before, we now contribute specific functional connections to focus on in future research.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"91"},"PeriodicalIF":7.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to Xing et al.: post-marketing safety concerns with Lecanemab: a pharmacovigilance study based on the FDA adverse event reporting system database.","authors":"Michael Irizarry, Ilona Surick, Ari Michael, Lynn D Kramer","doi":"10.1186/s13195-025-01735-5","DOIUrl":"https://doi.org/10.1186/s13195-025-01735-5","url":null,"abstract":"<p><p>A recent paper published a lecanemab analysis with data from the United States Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database. While the authors mention the limitations of FAERS, such as \"voluntary (underreporting), the inability to establish causality, reporting bias, data quality issues, and the absence of a denominator, which precludes calculating incidence rates\", they proceed with generalizations, clinical conclusions, and even treatment recommendations based on the crude disproportionality analysis. Consideration of post-marketing safety reports, including those found in the FAERS database, is an essential component of pharmacovigilance. However, FDA guidance [2, 3] highlights that: (1) \"Rates of occurrence cannot be established with reports,\" (2) \"Documenting one or more of these outcomes in a report does not necessarily mean that the suspect product(s) named in the report was the cause of the outcomes,\" and (3) \"Importantly, the FAERS data by themselves are not an indicator of the safety profile of the drug.\" The FAERS database includes reports from many sources, including reports by companies, as well as from health care professionals and consumers. The reports in the FDA database have significant limitations, including submission of incomplete, inaccurate, untimely, duplicate, relatedness to drug uncertainty, and/or unverified information. Therefore, broader generalizations, clinical conclusions, and treatment recommendations should not be made based solely on FAERS databases analyses.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"92"},"PeriodicalIF":7.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing midlife metabolic syndrome thresholds for dementia: a prospective study of two UK population-based cohorts.","authors":"Sam Vidil, Archana Singh-Manoux, Benjamin Landré, Aurore Fayosse, Séverine Sabia, Marcos D Machado-Fragua","doi":"10.1186/s13195-025-01732-8","DOIUrl":"https://doi.org/10.1186/s13195-025-01732-8","url":null,"abstract":"<p><strong>Background: </strong>The concept of metabolic syndrome (MetS) was developed to identify individuals at higher risk of type 2 diabetes and cardiovascular disease, but its relevance for dementia remains unclear. We examined MetS in midlife for association with late-onset dementia, focusing on the thresholds of MetS components that carry risk for dementia.</p><p><strong>Methods: </strong>MetS components (waist circumference, blood pressure, triglycerides, HDL-C, and fasting glucose) were measured on 6,137 white participants < 60 years from the Whitehall II (WII) cohort study. A changepoint method in time-to-event analyses was used to identify optimal thresholds, and those exhibiting better performance for dementia were retained to develop a revised MetS definition. Results were validated on 171,886 participants in the UK Biobank (UKB) study.</p><p><strong>Results: </strong>Over a median follow-up of 22.6 years in WII and 13.8 years in UKB, 522 and 418 late-onset dementia cases were recorded, respectively. Optimized thresholds for triglycerides and fasting glucose performed better than original MetS thresholds in WII, and were used to develop a revised MetS definition. The MetS scale had a linear association with dementia, and 1-component increment (range 0 to 5) was associated with higher dementia risk using the revised MetS definition (HR, 95% CI: 1.11, 1.03-1.19) but not the original MetS definition (HR, 95% CI: 1.06, 0.98-1.14) in WII. In UKB, the revised MetS definition exhibited better performance for dementia risk than the original definition (p for HR comparison < 0.01).</p><p><strong>Conclusions: </strong>MetS in midlife is potentially an important target for dementia prevention. However, the thresholds for triglycerides and glucose that carry risk need to be tailored specifically for dementia.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"89"},"PeriodicalIF":7.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12016442/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of choroid plexus volume with white matter hyperintensity volume and susceptibility and plasma amyloid markers in cerebral small vessel disease.","authors":"Pengcheng Liang, Meng Li, Yiwen Chen, Zhenyu Cheng, Na Wang, Yuanyuan Wang, Nan Zhang, Yena Che, Jing Li, Changhu Liang, Lingfei Guo","doi":"10.1186/s13195-025-01740-8","DOIUrl":"https://doi.org/10.1186/s13195-025-01740-8","url":null,"abstract":"<p><strong>Background: </strong>White matter hyperintensity (WMH) is a key feature of cerebral small vessel disease (CSVD). The impact of the choroid plexus (CP) volume on disease progression remains largely unexplored. This study evaluated the relationship between CP volume and CSVD severity via WMH volume and susceptibility values. Additionally, we explored whether Alzheimer's disease (AD)-related plasma proteins influence the volume of the CP.</p><p><strong>Methods and materials: </strong>Our study included 291 CSVD individuals, with 84 participants completing subsequent brain MRI at a mean follow-up of 20 months. To explore the potential CP-associated pathways, we assessed the relationships between AD-related plasma biomarkers and CP volume via multiple linear regression analysis. The longitudinal associations between CP volume and WMH characteristics (WMH volume and susceptibility) were analyzed via linear mixed-effects models. Finally, we employed random forest analysis with the Boruta algorithm to identify key predictors of CSVD severity.</p><p><strong>Results: </strong>Plasma Aβ1‒40 levels were positively correlated with CP volume (β = 0.115, P = 0.009), whereas Aβ42‒40 ratio were negatively associated with CP volume (β = -0.135, P = 0.03). Notably, increased CP volume was associated with both greater WMH burden (β = 0.191, P = 0.011) and decreased WMH susceptibility (β = -0.192, P = 0.012). Furthermore, random forest modeling identified CP volume and WMH susceptibility as the strongest predictors of CSVD severity.</p><p><strong>Conclusions: </strong>CP volume changes were significantly correlated with both WMH volume and WMH susceptibility in CSVD patients. These findings suggest that CP-mediated pathways may link amyloid metabolism to CSVD progression.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"90"},"PeriodicalIF":7.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12016351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation signature of a lifestyle-based resilience index for cognitive health.","authors":"Wei Zhang, David Lukacsovich, Juan I Young, Lissette Gomez, Michael A Schmidt, Eden R Martin, Brian W Kunkle, X Steven Chen, Deirdre M O'Shea, James E Galvin, Lily Wang","doi":"10.1186/s13195-025-01733-7","DOIUrl":"https://doi.org/10.1186/s13195-025-01733-7","url":null,"abstract":"<p><p>Cognitive resilience (CR) contributes to the variability in risk for developing and progressing in Alzheimer's disease (AD) among individuals. Beyond genetics, recent studies highlight the critical role of lifestyle factors in enhancing CR and delaying cognitive decline. DNA methylation (DNAm), an epigenetic mechanism influenced by both genetic and environmental factors, including CR-related lifestyle factors, offers a promising pathway for understanding the biology of CR. We studied DNAm changes associated with the Resilience Index (RI), a composite measure of lifestyle factors, using blood samples from the Healthy Brain Initiative (HBI) cohort. After corrections for multiple comparisons, our analysis identified 19 CpGs and 24 differentially methylated regions significantly associated with the RI, adjusting for covariates age, sex, APOE ε4, and immune cell composition. The RI-associated methylation changes are significantly enriched in pathways related to lipid metabolism, synaptic plasticity, and neuroinflammation, and highlight the connection between cardiovascular health and cognitive function. By identifying RI-associated DNAm, our study provided an alternative approach to discovering future targets and treatment strategies for AD, complementary to the traditional approach of identifying disease-associated variants directly. Furthermore, we developed a Methylation-based Resilience Score (MRS) that successfully predicted future cognitive decline in an external dataset from the Alzheimer's Disease Neuroimaging Initiative (ADNI), even after accounting for age, sex, APOE ε4, years of education, baseline diagnosis, and baseline MMSE score. Our findings are particularly relevant for a better understanding of epigenetic architecture underlying cognitive resilience. Importantly, the significant association between baseline MRS and future cognitive decline demonstrated that DNAm could be a predictive marker for AD, laying the foundation for future studies on personalized AD prevention.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"88"},"PeriodicalIF":7.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12016380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Investigating the Aβ and tau pathology in autosomal dominant Alzheimer's disease: insights from hybrid PET/MRI and network mapping.","authors":"Zhi Zhou, Qigeng Wang, Linwen Liu, Qi Wang, Xiaojun Zhang, Can Li, Jiajin Liu, Yidan Wei, Jin Gao, Liping Fu, Ruimin Wang","doi":"10.1186/s13195-025-01730-w","DOIUrl":"https://doi.org/10.1186/s13195-025-01730-w","url":null,"abstract":"","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"87"},"PeriodicalIF":7.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between blood pressure indicators and fluid biomarkers of brain aging in functionally intact older adults.","authors":"Anna M VandeBunte, Bailey L Ortiz, Emily W Paolillo, Rowan Saloner, Valentina Diaz, Shubir Dutt, Claire J Cadwallader, Coty Chen, Argentina Lario Lago, Julio C Rojas, Brandon Chan, Isabel Sible, Joel H Kramer, Kaitlin B Casaletto","doi":"10.1186/s13195-025-01731-9","DOIUrl":"https://doi.org/10.1186/s13195-025-01731-9","url":null,"abstract":"<p><strong>Background: </strong>Dementia risk is significantly shaped by cardiovascular health, with elevated blood pressure emerging as a key risk factor for adverse brain aging. Blood biomarkers such as pTau181, Aβ42/40, NfL, and GFAP have improved our understanding of dementia pathophysiology, however, few studies have explored how specific blood pressure metrics relate to biomarker levels, which could inform personalized dementia prevention strategies as these biomarkers move into clinic. We examined how different blood pressure metrics associated with molecular markers of astrocytic activation (GFAP), neuronal axon breakdown (NfL), and Alzheimer's disease pathobiology (pTau181, Aβ42/40) in plasma.</p><p><strong>Methods: </strong>109 functionally intact (Clinical Dementia Rating Scale = 0) older adults completed blood draws with plasma assayed for Aβ42/40, GFAP, NfL, and pTau181 (Quanterix Simoa) and in-lab blood pressure quantification. Blood pressure metrics included diastolic blood pressure, systolic blood pressure, and pulse pressure (systolic minus diastolic). Separate regression models evaluated plasma biomarkers as a function of each blood pressure metric, adjusting for age and biological sex. Interaction models tested whether relationships between blood pressure metrics and plasma biomarkers differed by sex, age, or APOE-ε4 status.</p><p><strong>Results: </strong>With the exception of Aβ42/40, higher pulse pressure related to higher levels of all plasma biomarkers examined (pTau181, NfL, GFAP). Additionally, higher systolic blood pressure related to higher pTau181, while diastolic blood pressure did not meaningfully associate with any biomarker. Interaction models revealed a significantly stronger relationship between elevated pulse pressure and higher GFAP concentrations in females compared to males, as well as a significantly stronger association between elevated pulse pressure and lower Aβ42/40 plasma concentrations in APOE-ε4 carriers compared to non-carriers.</p><p><strong>Conclusions: </strong>Our findings suggest that elevated pulse pressure, and to a lesser extent systolic blood pressure, are associated with increased Alzheimer's disease and neurodegenerative (axonal and astrocytic health) biology among typically aging adults. These associations underscore the importance of blood pressure management, particularly pulse pressure, for reducing dementia risk. Cardiovascular health may be incorporated with biomarkers to further personalize dementia prevention and management strategies.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"85"},"PeriodicalIF":7.9,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abdominal obesity and the risk of young-onset dementia in women: a nationwide cohort study.","authors":"Ye Seul Yang, Kyungdo Han, Dae Young Cheon, Minwoo Lee","doi":"10.1186/s13195-025-01738-2","DOIUrl":"10.1186/s13195-025-01738-2","url":null,"abstract":"<p><strong>Background and objectives: </strong>The association between obesity and young-onset dementia (YOD, defined as dementia diagnosed before age 65) is established, but the specific impact of abdominal obesity in women remains unclear. Abdominal obesity, driven by excess visceral fat, may increase dementia risk through metabolic and vascular pathways. We investigated the association between abdominal obesity and YOD risk in women using a large nationwide cohort.</p><p><strong>Methods: </strong>We analyzed 964,536 Korean women aged 40-60 years who underwent national health checkups in 2009. General obesity was defined by body mass index (BMI), and abdominal obesity was categorized by waist circumference (WC) into < 75 cm, 76-84 cm, 85-94 cm, and ≥ 95 cm. YOD was identified using ICD-10 codes and dementia medication prescriptions. Hazard ratios (HRs) for YOD were estimated using multivariable Cox proportional hazard models adjusted for lifestyle and clinical factors.</p><p><strong>Results: </strong>Over a median follow-up of 8.2 years, YOD incidence increased progressively with higher WC. Women with WC ≥ 95 cm had a 55% increased risk of YOD (HR 1.55; 95% CI 1.34-1.79) compared to those with WC < 75 cm. The association was particularly strong for vascular dementia (VD), with HR 1.83 (95% CI 1.30-2.57). By contrast, BMI showed a U-shaped relationship, with the lowest YOD risk observed in women with normal BMI (18.5-22.9 kg/m²), and significantly elevated risks in both underweight (BMI < 18.5 kg/m²; HR 1.39, 95% CI 1.13-1.71) and morbidly obese women (BMI ≥ 30 kg/m²; HR 1.26, 95% CI 1.10-1.45).</p><p><strong>Discussion: </strong>Abdominal obesity is a significant, independent risk factor for YOD in women, particularly for VD. These findings underscore the importance of addressing abdominal obesity in middle-aged women to reduce dementia risk.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"86"},"PeriodicalIF":7.9,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of nucleos(t)ide analogue therapy on the incidence of Alzheimer's disease in patients with chronic hepatitis B virus infection.","authors":"Jihye Lim, Hyundam Gu, Hyunji Sang, Su Jin Jeong, Ha Il Kim","doi":"10.1186/s13195-025-01729-3","DOIUrl":"https://doi.org/10.1186/s13195-025-01729-3","url":null,"abstract":"<p><strong>Background: </strong>Long-term therapy with nucleos(t)ide analogs (NUCs) is inevitable for chronic hepatitis B (CHB) patients. However, how NUC therapy on the developing Alzheimer's disease (AD) in these patients remains controversial.</p><p><strong>Methods: </strong>This retrospective cohort study used the Korean National Health Insurance Service claims database from January 1, 2013, to December 31, 2013, treatment naïve CHB patients and those without previously diagnosed with AD. Participants were followed from the index date until either the diagnosis of AD or the study's conclusion on December 31, 2021. The primary outcome was the incidence of AD, compared between the group with initiated NUC therapy (n = 18,365) at cohort entry and the group without NUC therapy (n = 212,820).</p><p><strong>Results: </strong>During the study, 416 patients were diagnosed with AD. After propensity-score matching (18,365 pairs), the 5- to 7-year follow-up showed a significantly lower hazard ratio (HR) in the NUC-treated group compared to the untreated group (HR 0.31-0.40), with HRs remaining constant over time. Subgroup analysis showed more pronounced benefits of NUC therapy in patients under 65 years (HRs: 0.22 vs. 1.23; P < 0.05) and those without dyslipidemia (HRs: 0.14 vs. 1.09; P < 0.05). Protective effects were also observed across subgroups with hypertension, chronic kidney disease, heart disease, and a history of brain trauma, consistent with AD risk factor trends.</p><p><strong>Conclusions: </strong>Our study analyses suggest that NUC therapy appears to have a protective effect against the development of AD in patients with CHB.</p>","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"84"},"PeriodicalIF":7.9,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: γ‑Secretase modulator resistance of an aggressive Alzheimer‑causing presenilin mutant can be overcome in the heterozygous patient state by a set of advanced compounds.","authors":"Johannes Trambauer, Rosa Maria Rodriguez Sarmiento, Holly J Garringer, Katja Salbaum, Liliana D Pedro, Dennis Crusius, Ruben Vidal, Bernardino Ghetti, Dominik Paquet, Karlheinz Baumann, Lothar Lindemann, Harald Steiner","doi":"10.1186/s13195-025-01723-9","DOIUrl":"https://doi.org/10.1186/s13195-025-01723-9","url":null,"abstract":"","PeriodicalId":7516,"journal":{"name":"Alzheimer's Research & Therapy","volume":"17 1","pages":"83"},"PeriodicalIF":7.9,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12001704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}