The new study by the University of Minnesota shows that an Alzheimer’s-related gene is not necessary to protect against the disease, and may actually be harmful to people who already have it.
The findings have been hailed as an important step forward in understanding how the disease progresses.
The new findings, published in the journal Cell, show that a gene called the CRISPR-Cas9 protein is a major driver of Alzheimer’s, and that this protein can prevent the disease from forming.
In the new study, scientists at the university examined gene activity from the brain of patients with Alzheimer’s disease who had their brains destroyed.
The CRISP gene was not activated by the blast of DNA in the brain, but was activated by an engineered protein that contained a gene from the CRPS gene.
This modified protein was able to prevent the CRisPR-cas9 protein from binding to the gene in the damaged brain, thereby preventing it from binding and causing the damage to occur.
Researchers found that the CRIsPR-sDNA binding activity was not as potent as the CRSPS gene activity, but the CRASP protein was significantly more potent, leading to a 50 percent increase in the CRAsPs binding activity compared to the CRDSP gene activity.
These findings may have significant implications for Alzheimer’s research, since it suggests that the gene activity of the CRP gene may also be a factor in causing the disease.
“This gene activity may play a role in Alzheimer’s development, but also in its progression,” said lead author Kristine Liss-Riordan, a postdoctoral researcher in the Department of Biological Engineering.
The researchers believe that the increased CRISPAR-sRNA binding activity is probably due to the increase in expression of the protein that was generated by the CRSP gene, which is a member of the Cas9 family of genes.
They also discovered that the activity of this gene was increased when the CROSPR-cDNA binding protein was added to the brain.
The results suggest that the Cas1 protein was activated during the damage, but that the proteins of the two other Cas proteins, Cas9a and Cas9b, are responsible for the activation of the other gene.
The work was supported by the National Institutes of Health, the National Science Foundation, the John D. and Catherine T. MacArthur Foundation, and the Swedish Research Council.
Liss -Riordon is now working with researchers at the National Institute of Neurological Disorders and Stroke (NINDS) to explore the possible effects of CRISPER-Cas11 on other gene expression patterns in other cells, including neurons.
The next step will be to test whether the CRIST-Cas1 protein also activates other gene transcription factors in the developing brain, such as CREB, in animals, Liss said.
This research was supported in part by the NINDS Biomedical Research Initiative, and by the Charles and Helen DeVos Fund for Advanced Research.
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