Two cancer medications are promising when reverting the devastating Alzheimer’s effects

Two cancer medications could potentially decrease or even reverse the effects of Alzheimer’s disease, suggests a new study.

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

Then, they observed what existing medications approved by the FDA could counteract or reverse those changes.

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

Medications, Letrozone and Iinotecan are approved to treat cancer. Letrozole is a medication for breast cancer and Iinotecan treats colon and lung cancer.

When the scientists tested a combination of both medications in mice, they noticed a reversal of the changes of gene expression that were initiated by Alzheimer’s.

They also discovered a reduction in Tau protein groups in the brain, a key score of Alzheimer, and an improvement in learning and memory.

“Alzheimer’s disease comes with complex changes in the brain, which has made it difficult to study and treat, but our computational tools opened the possibility of addressing complexity directly,” said the co-senior author Marina Sirota, PHD, interim director of the Institute of Computational Health Sciences of the UCSF Bakar and Pediatrics professor, in the press release.

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“We are excited that our computational approach has led us to a possible combination therapy for Alzheimer’s based on existing medications approved by the FDA.”

The results of the study, which was financed by the National Institutes of Health (NIH) and the National Science Foundation, were published in Cell magazine on July 21.

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

They also noticed that animal models were used.

“Although necessary, validation in animal models can not completely recapitulate human biology,” the researchers wrote.

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There was also a notable gender difference in response to medications, and male mice responded better than women.

“As a hormonal modulator, Lartazole could contribute to this sex difference,” the team said. “However, the analysis remains non -conclusive due to the small number of male letrozole users.”

Electronic medical records could also present limitations, “since the data tends to be scarce and are not collected with a specific investigation in mind.”

“We hope that this can be translated rapidly to a real solution for millions of patients with Alzheimer’s.”

According to the Association of the Alzheimer’s Association, more than seven million people in the United States live with Alzheimer’s.

This number is expected to approach 13 million by 2050.

Currently there are only two disease -modifying medications that have been approved by the FDA to treat Alzheimer, declares UCSF.

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

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They work by reducing the accumulation of amyloid plaques in the brain, but they are only effective for those with an early stage and have the potential of some serious side effects, according to experts.

(Other Alzheimer’s medications help with symptoms, but do not treat the underlying disease).

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“Alzheimer’s is probably the result of numerous alterations in many genes and proteins that, together, interrupt the health of the brain,” said Co-Senior study author Yadong Huang, MD, PHD, professor of neurology and pathology at UCSF, in the launch.

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

Looking towards the future, researchers plan to start a clinical trial to explore the impact of combined medications in human patients with Alzheimer’s.

“If completely independent data sources, such as individual cell expression data and clinical records, guide us to the same ways and the same medications, and then solve the Alzheimer’s in a genetic model, then perhaps we are in something,” Sirota said in the statement.

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“We hope that this can be translated rapidly to a real solution for millions of patients with Alzheimer’s.”