Abstract The apolipoprotein E ε4 ( APOE4 ) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet the mechanistic underpinnings by which it alters human microglial function remain poorly understood. Here, we utilize CRISPR/Cas9-engineered isogenic human induced pluripotent stem cell-de...
T. Ikezu, Y. You, Son Nguyen et al.· Research Square· 0 citations
The complement system, a proteolytic cascade crucial for innate immune system function, is dysregulated in brain aging and neurodegenerative diseases, including Alzheimer Disease (AD). In models of AD, complement proteins, including C1q and C3, are upregulated and mediate microglial clearance of amyloid plaques and pru...
C. Nadarajah, Michelle Y. Li, Sohui Park et al.· bioRxiv· 0 citations
Tauopathies are characterized by the accumulation and spread of pathogenic tau aggregates throughout the brain, a process that is increasingly recognized to involve not only neurons but also microglia. However, whether pathogenic MAPT directly alters microglial degradative capacity remains poorly understood. Here, usin...
Kylie J. Schache, Rui Zhang, Audrey Street et al.· bioRxiv· 0 citations
INTRODUCTION Microglia regulate amyloid plaque-associated microenvironments that contribute to downstream tau pathology in Alzheimer’s disease (AD). Variants within the MS4A locus are strongly associated with AD risk and resilience and are linked to microglial biology; however, the functional role of MS4A4A in plaque-a...
E. Danhash, Shao-Yu Fang, Jacob A. Marsh et al.· bioRxiv· 0 citations
Findings identify widespread lncRNA dysregulation across neural cell types in the setting of a MAPT mutation and nominate the NORAD-pumilio axis as a regulatory pathway linking RNA homeostasis and tau propagation biology.
Joseph E. Zemke, Guangming Huang, Emma Starr et al.· bioRxiv· 0 citations
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