ArticleScientific reports2022
Glycosylated clusterin species facilitate Aβ toxicity in human neurons.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Plasma clusterin levels in autism spectrum disorder: bridging biomarkers to social and cognitive dysfunctions.BMC pediatrics · 2026Article
- FGF13 is not secreted from mouse neurons.JCI insight · 2026Article
- Changes in iPSC-astrocyte morphology reflect Alzheimer's disease patient clinical markers.Stem cells (Dayton, Ohio) · 2025Article
- Brain and plasmatic CLUSTERIN are translational markers of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- The decreased astrocyte-microglia interaction reflects the early characteristics of Alzheimer's disease.iScience · 2024Article
- Glycoproteomics in Cerebrospinal Fluid Reveals Brain-Specific Glycosylation Changes.International journal of molecular sciences · 2023Article
- Clusterin/apolipoprotein J, its isoforms and Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clusterin (CLU) is one of the most significant genetic risk factors for late onset Alzheimer's disease (AD). However, the mechanisms by which CLU contributes to AD development and pathogenesis remain unclear. Studies have demonstrated that the trafficking and localisation of glycosylated CLU proteins is altered by CLU-AD mutations and amyloid-β (Aβ), which may contribute to AD pathogenesis. However, the roles of non-glycosylated and glycosylated CLU proteins in mediating Aβ toxicity have not been studied in human neurons. iPSCs with altered CLU trafficking were generated following the removal of CLU exon 2 by CRISPR/Cas9 gene editing. Neurons were generated from control (CTR) and exon 2 -/- edited iPSCs and were incubated with aggregated Aβ peptides. Aβ induced changes in cell death and neurite length were quantified to determine if altered CLU protein trafficking influenced neuronal sensitivity to Aβ. Finally, RNA-Seq analysis was performed to identify key transcriptomic differences between CLU exon 2 -/- and CTR neurons. The removal of CLU exon 2, and the endoplasmic reticulum (ER)-signal peptide located within, abolished the presence of glycosylated CLU and increased the abundance of intracellular, non-glycosylated CLU. While non-glycosylated CLU levels were unaltered by Aβ
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