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Korin Miller

Researchers Have Discovered BRCA1 Link to Alzheimers

Korin Miller
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New research has found that depletion of the body’s levels of BRCA1, which is famously linked to several forms of cancer, may also cause dementia. (Corbis)

It’s already known – primarily due to Angelina Jolie’s announcement that she has it – that certain mutations in BRCA1, an important protein involved in DNA repair, can increase a person’s risk of developing breast and ovarian cancer, but researchers from the University of California and Gladstone Institute of Neurological Disease have found that it’s also linked to Alzheimer’s disease.

In a study published in the journal Nature Communications, scientists experimentally reduced BRCA1 levels in the neurons (cells that transmit nerve impulses) of mice. They discovered that the mice had learning and memory issues as a result.

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Researchers then studied BRCA1 levels in post-mortem brains of human Alzheimer’s patients and found that the levels were reduced by 65 to 75 percent, as compared with patients that didn’t have dementia.

To figure out why this depletion happens, researchers then grew neurons in a lab and treated them with amyloid-beta proteins, which accumulate in the brains of people with Alzheimer’s. The proteins depleted BRCA1 levels.

What does this mean, exactly? BRCA1 is important for our brains to function properly, and Alzheimer’s disease depletes the levels of the protein in our brains, making it difficult for them to work the way that they should.

Related: ‘I Am Now In Menopause’: Angelina Jolie Reveals

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The work is the latest to emphasize the importance of functional BRCA1 for our overall health.

According to the National Cancer Institute, up to 65 percent of women who inherit a particular BRCA1 mutation will develop breast cancer by age 70 and 39 percent of women with the mutation will develop ovarian cancer by that age. The mutation may also increase a woman’s risk of developing fallopian tube cancer and a man’s risk of prostate and pancreatic cancer.

Study co-author Lennart Mucke, MD, director of the Gladstone Institute of Neurological Disease, tells Yahoo Health that he’s excited by the findings. “Our study demonstrates for the first time, when one looses BRCA1 in nerve cells, they don’t like that very much,” he says. “It seems pretty clear that BRCA1 functions in support of cognitive functions in the brain.”

Other neurologists are taking note. Clifford Segil, DO, a neurologist at California’s Providence Saint John’s Health Center tells Yahoo Health that the latest findings are “fascinating,” adding that he’s happy people are trying to link oncology and neurology.

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However, Segil says, he’s seen this sort of thing before. “Unfortunately, we’ve had similar findings in the past that haven’t translated into medications for patients,” he says. “We’re finding things that are risk factors but they don’t help us find a new diagnostic tool or clinical therapy.”

According to the Alzheimer’s Association, Alzheimer’s disease is the only top 10 cause of death in America that can’t be prevented, cured, or slowed down. An estimated 5.1 million people aged 65 and older suffer from the disease, and that number is expected to increase to 7.1 million by 2025.

Related: This Woman Explains What It’s Like to Be in a Medically Induced Coma

But Mucke says that the latest findings might eventually lead to the use of BRCA1 therapy to increase levels of the proteins to prevent or reverse neurodegenerative issues. However, he adds, that’s “a ways away.”

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Mucke notes that women who have the BRCA1 mutation aren’t necessarily at a greater risk of developing Alzheimer’s disease. “There is no evidence that we’re aware of that BRCA1 mutations increase the risk for Alzheimer’s disease,” he says. “It may be easier for the brain to compensate for BRCA1 deficiencies early in life.”

Segil says he’s cautiously optimistic that the latest discovery may lead to new treatment for his patients. “It’s too simplistic to think that one protein is responsible for Alzheimer’s,” he says. “I’m always optimistic that this will be the protein that changes treatment but unfortunately, that hasn’t happened yet.”

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