Reverse Alzheimer’s damage: Two cancer properties show a sudden force
UC San Francisco and Gladstone scientists have identified cancer medications that are contrary to the changes in the brain during Alzheimer’s disease, and may slow down or even reflect their symptoms.
The study first analyzed how Alzheimer’s disease changed genetic expression in the individual cells in the human brain. After that, researchers researched the existing drugs that have already been approved by the Food and Drug Administration (FDA) and causing contrast changes in genetic expression.
They were specifically looking for medications that would reflect the changes in genetic expression in neurons and in other types of brain cells called GLIA, all of which were damaged or changed in Alzheimer’s disease.
After that, the researchers analyzed millions of electronic medical records to show that patients who took some of these medications as part of their treatment of other cases were less likely to develop Alzheimer’s disease.
When they tested a mixture of upper drugs – both of them are cancerous drugs – in the mouse model for Alzheimer’s mouse, it reduced the brain degeneration in mice, and even restore their ability to remember.
“Alzheimer’s disease comes with complex changes on the brain, which made it difficult to study and treat, but our calculations have opened the possibility of the Institute for Computer Health in UCSF Bakar, professor of pediatrics, and the temporary author of the paper.” We are excited because our arithmetic approach prompted us to treat a potential mix of Alzheimer’s disease based on current medicines Approved by the Food and Drug Administration. “
The results appeared in cell On July 21. The research was partially funded by the National Institutes of Health and the National Science Corporation.
Large data from patients and cells indicate the treatment of new Alzheimer’s disease
Alzheimer’s disease affects 7 million people in the United States and causes uncompromising decrease in perception, learning and memory. However, contracts of research produced only two accredited properties from the FDA (FDA), neither of them can slow down this decline useful.
“It is possible that Alzheimer’s is likely to be the result of many adjustments in many genes and proteins that have disrupted brain health together,” said Yadong Huang, PhD, the first researcher at the paper center in Gladiston, Professor of Neuroscience at UCSF, and co -author of the co -sheet of the paper. “This makes it very difficult to develop the drug – which traditionally produces one medicine for one gene or one protein that pushes the disease.”
The team took data available to the public from three studies on Alzheimer’s brain that measures the genetic expression of one cell in the brain cells from the died donors with or without Alzheimer’s disease. They used this data to produce genetic expression signatures for Alzheimer’s disease in neurons and Sex.
The researchers compared these signatures with those in the communication map, which is a database of results from testing the effects of thousands of medications on genetic expression in human cells.
Of the 1300 drugs, 86 reversed the signature of the genetic expression of Alzheimer’s disease in one type of cell, and 25 opposite the signature in many types of cells in the brain. But only 10 was approved by the Food and Drug Administration for Human use.
Through the records in the University of California’s healthy data warehouse, which includes unidentified health information on 1.4 million people over the age of 65, the group found that many of these drugs have reduced the risk of developing Alzheimer’s disease over time.
“Thanks to all these current data sources, we have moved from 1300 drugs, to 86, to 10, to 5,” said Yaqiao Li, a PhD, a former student student at the Serotta Laboratory, who is now a post -PhD researcher at the Huang Laboratory in Glagston and the main author of the paper. “In particular, we have indicated the rich data collected by all the University of California’s health centers to the most promising drugs. It is a type of fake clinical experience.”
Treatment of a mixture prepares for a quiet time
Li, Huang and Sirota chose two cancer drugs among the 5 best drug candidates for laboratory tests. And expect one drug, a liter, will be treated with Alzheimer’s disease in neurons. Another, Irinotecan, would help perfection. Letrozole is usually used to treat breast cancer. Irinotecan is usually used to treat colon and lung cancer.
The team used the mouse model for the aggressive Alzheimer’s disease with multiple mutations associated with the disease. With the appearance of advanced mice, symptoms similar to Alzheimer’s disease appeared, and they were treated with drugs or both.
The combination of cancer real estate was reflected in multiple aspects of Alzheimer’s disease in the animal model. The signatures of genetic expression in neurons and crimes that appeared with the progress of the disease have been removed. He reduced the formation of toxic blocks of proteins and brain degradation. More importantly, he regained memory.
“It is extremely exciting to see the validity of the arithmetic data in the widely used Alzheimer’s mouse model,” said Huang. The research is expected to soon apply to a clinical trial so that the team can test the compound treatment directly in Alzheimer’s patients.
“If the sources of data are completely independent, such as one expression and clinical records, we went to the same paths and the same drugs, then the Alzheimer’s disease resolved in a genetic model, then we are on something,” said Serotta. “We hope this will quickly be translated into a real solution for millions of patients with Alzheimer’s disease.”
Authors: The other UCSF authors are Carloota Perida Serra, MS, Jessica Bluminfeld, Xinyu Tang, PhD, Antara Rao, PhD, Sarah and Wolmeram, PhD, Alice Tang, PhD, Tomico Oscotsky, MD, Michael J Keser, PHD. The author of other Gladstone institutes are Min XIE, PHD, Yanxia Hao, Elise Deng, Young CHUN, Julia Holtzman, ALICE ANI and Seo Yoon Yoon, MBA, Alex Zhang, Jeffrey Simms, MA and Iris Lo.
Funding: This study was supported by the National Institute of Ouar (R01ag0393, R01ag057683, RF1AG07647, R01ag078164, P01ag073082), National Science Foundation (2034836) and the Dolby Family Fund.
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