Two cancer medications show a promise to reverse Alzheimer’s devastating effects

A new study may be that two cancer drugs can delay or even reverse the effects of Alzheimer’s disease.

Researchers at the University of California San Francisco (UCSF) explored how common dementia changes gene expression (which genes are lit or turned off) in certain brain cells, according to a university statement.

They then noticed which existing drugs approved by the FDA could counteract or reverse these changes.

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When analyzing millions of electronic medical records of adults over 65, researchers identified two medicines that seemed to reduce the likelihood of Alzheimer’s in the patients who took them.

Medicines (Letrozone and Irinotecan) are approved to treat cancer. Letrozol is a medication against breast cancer and Iinotecan deals with colon and lung cancer.

When scientists tried a combination of both medicines in mice, they observed a reversal of the gene expression changes initiated by Alzheimer’s.

They also discovered a reduction in TAU proteins in the brain, a key marker of Alzheimer’s, and an improvement in learning and memory.

“ Alzheimer’s disease involves complex changes in the brain, which has made it difficult to study and treat, but our computational tools opened the possibility of directly dealing with complexity, ” said Co -enior Marina Sirota, a doctor, the interim director of the UCSF Bakar Computational Institute Institute and Pediatrics Professor, in the press release.

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“We are excited that our computational approach has led us to potential combined therapy for Alzheimer’s based on existing medicines approved by the FDA.”

The results of the study, partly funded by the National Health Institutes (NIH) and the National Science Foundation, were published in Cell Magazine on July 21.

Although the result of the study was promising, researchers recognized several limitations, including the fact that the database they used to identify possible drugs was built from cancer cells, not brain cells.

They also said that animal models were used.

“Although necessary, validation in animal models may not fully recapture human biology,” researchers wrote.

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There was also a remarkable gender difference in response to medicines, with male mice that responded better than women.

“As a hormonal modulator, Letrozole can contribute to this sex difference,” the team said. “However, the analysis is still inconclusive due to the small number of letrozol male users.”

Electronic medical records could also have limitations, “as data are usually scarce and not collected taking into account specific research.”

“We hope this will be quickly translated into a real solution for millions of patients with Alzheimer’s.”

Currently, more than seven million people live with Alzheimer’s, according to the Alzheimer’s Association.

This number is expected to approach 13 million in 2050.

Currently, there are only two disease modifying drugs that have been approved by the FDA to treat Alzheimer’s, says the UCSF.

Lecanemab (Leqembi) and Donanemab (Kisunla) are monoclonal antibodies that are administered by IV infusions.

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They work by reducing the accumulation of amyloid plates in the brain, but are only effective for those with Alzheimer’s in the initial phase and have the potential of some serious side effects, according to experts.

(Other Alzheimer’s drugs help symptoms but do not treat underlying disease.)

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“Alzheimer’s is probably the result of numerous alterations in many genes and proteins that, together, disrupt brain health,” said the author of the Co -enior Yadong Huang, MD, doctor, professor of neurology and pathology at the UCSF, in the statement.

“This makes it very difficult for drug development, which traditionally produces a drug for a single gene or protein that promotes the disease.”

In front, researchers are planning to start a clinical trial to explore the impact of combined medicines on human patients with Alzheimer’s.

“If completely independent data sources, such as cell expression data and clinical records, guide us towards the same roads and drugs, and then solve Alzheimer’s in a genetic model, we may be in something,” Sirota said in launch.

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“We hope this will be quickly translated into a real solution for millions of patients with Alzheimer’s.”