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PILRA (rs1859788 A > G) has been suggested to be a protective variant for Alzheimer's disease (AD) and is an entry co-receptor for herpes simplex virus-1. We conducted a nested case-control study of 360 1:1-matched AD subjects. Interactions between the PILRA-A allele, APOE risk variants (ε3/ε4 or ε4/ε4) and GM17 for AD risk were modelled. The associations were cross-validated using two independent whole-genome sequencing datasets. We found negative interactions between PILRA-A and GM17 (OR 0.72, 95% CI 0.52-1.00) and between PILRA-A and APOE risk variants (OR 0.56, 95% CI 0.32-0.98) in the discovery dataset. In the replication cohort, a joint effect of PILRA and PILRA × GM 17/17 was observed for the risk of developing AD (p .02). Here, we report a negative effect modification by PILRA on APOE and GM17 high-risk variants for future AD risk in two independent datasets. This highlights the complex genetics of AD.
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http://dx.doi.org/10.1038/s41598-022-17058-6 | DOI Listing |
Mol Nutr Food Res
September 2025
Department of Epidemiology and Health Statistics, School of Public Health, Qingdao University, Qingdao, China.
The relationship between dietary biotin intake and cognitive function remains unclear. This study explores the association between biotin and dementia, and the mediating role of inflammation indicators. Dietary biotin intake was assessed via the 24-h recall questionnaire.
View Article and Find Full Text PDFMol Psychiatry
September 2025
Institute of Neurology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, 610054, China.
Alzheimer's disease (AD), a leading cause of dementia, represents a critical unmet global medical need. While the precise mechanisms underlying AD pathogenesis remain elusive, increasing evidence underscores the pivotal role of neuroinflammation in driving cognitive impairment. N6-methyladenosine (m6A), an epigenetic modification regulating RNA metabolism, has been found to be dysregulated in AD.
View Article and Find Full Text PDFGeroscience
September 2025
Department of Biological Sciences, College of Natural Sciences, Kangwon National University, Kangwon, 24341, Republic of Korea.
Alzheimer's disease (AD) represents a growing global health burden, underscoring the urgent need for reliable diagnostic and prognostic biomarkers. Although several disease-modifying treatments have recently become available, their effects remain limited, as they primarily delay rather than halt disease progression. Thus, the early and accurate identification of individuals at elevated risk for conversion to AD dementia is crucial to maximize the effectiveness of these therapies and to facilitate timely intervention strategies.
View Article and Find Full Text PDFJ Am Med Dir Assoc
September 2025
Department of Public Health Sciences, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA. Electronic address:
Objectives: In 2017, the Chronic Condition Warehouse released a 30-condition Chronic Condition file (CC30), which fully replaced the prior 27-condition file (CC27) in 2022. CC30 shortened the look-back period for dementia identification from 3 to 2 years and raised the required outpatient/carrier claims from 1 to 2. This change may disproportionately affect individuals with limited access to health care.
View Article and Find Full Text PDFMol Cell Neurosci
September 2025
Biomedical and Forensic Science, School of Human Sciences, University of Derby, Derby, DE22 1GB, United Kingdom; Life and Health Sciences, University of Roehampton, London, SW15 5PH, United Kingdom. Electronic address:
Emerging evidence indicates that apelin, an adipokine, plays a critical role in numerous biological functions and may hold potential for therapeutic applications; however, its efficacy is constrained by rapid plasma degradation. Thus, the search for novel apelin analogues with reduced susceptibility to plasma degradation is ongoing. We have previously shown novel modified apelin-13 analogues, providing exciting opportunities for potential therapeutic development against Alzheimer's disease.
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