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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Various studies indicated that the immune system is a cardinal feature of Alzheimer's disease (AD), which can either ameliorate or exacerbate AD neuropathogenesis. Nevertheless, the associations between genes involved in the immune system and AD remain unclear.
Method: To systematically evaluate the associations of these genes with AD, we investigated 370 genes implicated in the immune system based on previous studies selected using the PubMed database.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Article Synopsis
- Researchers have identified genetic polymorphisms of ABI3 as a risk factor for late-onset Alzheimer's Disease (LOAD), but the role of ABI3 in microglia is not well understood.
- Using CRISPR/Cas9, a specific risk variant (S212F) was introduced into mouse models to study its effects on AD-related pathologies alongside 5xFAD mice over time.
- Results showed that the 5xFAD/Abi3 mice exhibited a decrease in amyloid beta plaque burden and a significant reduction in microglia numbers with age, suggesting ABI3 may influence both plaque formation and microglial response in AD pathology.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Xiangya Hospital, Central South University, Changsha, Hunan, China.
Background: Genetics plays an important role in dementia with Lewy bodies (DLB) and remains poorly understood. Previous research has identified several genes associated with DLB, including APOE, GBA, SNCA, BIN1, TMEM175, PLCG2, and CNTN1. To date, genetic studies on DLB have focused on Caucasian population.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Background: New methods developed to estimate when AD biomarkers became abnormal in individuals have shown considerable heterogeneity in amyloid and tau pathology onset age. This work used polygenic scores (PGS) generated from CSF Aβ and ptau GWAS, individual-level genetic data, and estimated tau onset age (ETOA) to identify genetic influences on tau onset beyond APOE.
Method: Participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) with genetic data, CSF biomarkers (Aβ and ptau), and longitudinal [F]Flortaucipir (FTP) tau PET were analyzed (N = 462).
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Department of Population and Quantitative Health Sciences, Institute for Computational Biology, Case Western Reserve University, Cleveland, OH, USA.
Background: Many independent studies have found rare variants associated with AD. Current gene-based tests for rare-variants generally consider the impact of low-frequency coding variants as an independent effect from the common regulatory variants that surround them. In this work, we propose to increase the statistical power of kernel-based rare-variant association tests by accounting for the surrounding cis-regulatory variants' effects on gene expression.
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