Sourced from the University of Tokyo.
Experts at the University of Tokyo have identified a new protein in the pathway that leads to Alzheimer’s disease. Researchers used the “molecular scissors” of CRISPR/Cas9 to search for new genes related to the neurodegenerative disease.
The exact causes of Alzheimer’s disease remain unknown, but one of the most well- supported theories focuses on a protein called amyloid beta. Aggregation, or clumping together, and the depositing of two proteins, amyloid beta and tau, throughout a patient’s brain are a signature of Alzheimer’s disease.
CRISPR/Cas9 allows scientists to make specific changes to the DNA inside cells. Researchers used the CRISPR/Cas9 system to delete individual genes in mouse cells growing in a dish and then measured the amount of amyloid beta that the cells produced.
“We believe this is the first time anyone has used this CRISPR/Cas9 genetic screening technique to look for changes in amyloid beta production,” said Yukiko Hori, a co-first author on the research paper published in FASEB Journal and lecturer at the University of Tokyo.
Researchers tested a total of 19,150 individual genes for their effect on amyloid beta levels and ruled out all but one: calcium and integrin-binding protein 1 (CIB1).
Cells without functional CIB1 genes produced abnormally high levels of amyloid beta protein.
“Nobody knows why the deposition of amyloid beta occurs in Alzheimer’s disease patients’ brains, but we think a starting point of the process could be CIB1,” said Professor Taisuke Tomita, an expert in pathological biochemistry at the University of Tokyo and leader of the research lab that performed the study.
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