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Related Experiment Video

Updated: May 14, 2026

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

Published on: June 24, 2025

Genome-Wide CRISPR Screening Identifies Genetic Modulators of Amyloid Precursor Protein Processing.

You Li^1,2,3,4, Yingjia Yao^1,2,3,4, Zitao Xu^1,2,3,4

¹Interdisciplinary Research Center for Brain-Computer Interface, Key Laboratory of Bioresource Research and Development of Liaoning Province, College of Life and Health Sciences, Northeastern University, Shenyang 110819, China.

International Journal of Molecular Sciences

|May 13, 2026

Summary

Researchers identified new genes regulating amyloid precursor protein (APP) processing in Alzheimer's disease (AD). This discovery offers potential therapeutic targets by understanding APP cleavage and its links to cellular metabolism and trafficking.

Keywords:

APP processing Alzheimer’s disease CRISPR screen LDHB PIAS2 amyloid precursor protein cellular metabolism post-translational modification

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Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

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Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Genome-Wide CRISPR Screen for Unveiling Radiosensitive and Radioresistant Genes

Published on: May 23, 2025

Area of Science:

Neuroscience
Genetics
Molecular Biology

Background:

Proteolytic processing of amyloid precursor protein (APP) is central to Alzheimer's disease (AD) pathogenesis.
The complete genetic regulatory networks controlling APP cleavage remain largely uncharacterized.

Purpose of the Study:

To systematically identify novel regulators of APP cleavage using a genome-wide screen.
To uncover genetic modulators of both amyloidogenic and non-amyloidogenic APP processing pathways.

Main Methods:

Genome-wide CRISPR/Cas9 knockout screen with a UAS-GAL4-based cellular reporter.
Biochemical validation of identified gene candidates.
Integration with human AD transcriptomic datasets.

Main Results:

Identification of distinct functional gene clusters regulating APP processing, including those involved in cellular metabolism, protein modification, and vesicular trafficking.
Pinpointing of specific novel modulators: LDHB, PIAS2, CCDC53, and TRIM61.
Confirmation that ablating these genes alters the balance of sAPPα and amyloid-β (Aβ) production.
Demonstration of significant dysregulation of these modulators in human AD patient transcriptomic data.

Conclusions:

Establishment of a reporter-based screening framework for APP processing.
Identification of novel candidate genes (LDHB, PIAS2, CCDC53, TRIM61) linked to metabolism, protein modification, and vesicular trafficking as regulators of APP cleavage.
These findings provide a valuable resource for future mechanistic studies in Alzheimer's disease models.