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An Insertion Within SIRPβ1 Shows a Dual Effect Over Alzheimer’s Disease Cognitive Decline Altering the Microglial Response

JOURNAL OF ALZHEIMERS DISEASE. 2024-02; 
José María García-Alberca, Itziar de Rojas, Elisabeth Sanchez-Mejias , Diego Garrido-Martín
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Gene Synthesis Plasmids were designed in silico overthe pCDNA3.0 backbone and obtained from Genscript (www.genscript.com) Get A Quote

摘要

Background: Microglial dysfunction plays a causative role in Alzheimer's disease (AD) pathogenesis. Here we focus on a germline insertion/deletion variant mapping SIRPβ1, a surface receptor that triggers amyloid-β(Aβ) phagocytosis via TYROBP. Objective: To analyze the impact of this copy-number variant in SIRPβ1 expression and how it affects AD molecular etiology. Methods: Copy-number variant proxy rs2209313 was evaluated in GERALD and GR@ACE longitudinal series. Hippocampal specimens of genotyped AD patients were also examined. SIRPβ1 isoform-specific phagocytosis assays were performed in HEK393T cells. Results: The insertion alters the SIRPβ1 protein isoform landscape compromising its ability to bind... More

关键词

Alzheimer’s disease; DAP12; SIRPβ1; TREM2; TYROBP; copy-number variant; microglia.