The results showed a build up of DNA damage, leading to a decrease in learning and memory. Ironically, the gene also restores damaged DNA. If DNA is not repaired properly then it cells have more chances to develop additional genetic alterations raising the chance of developing breast and ovarian cancers. However, mutated BRCA1 gene is linked to both ovarian and breast cancers. The substance in question is breast cancer factor 1, known as BRCA1. Jolie opted to have a double mastectomy and her ovaries removed to avoid developing the disease.
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The Alzheimer’s finding makes sense, said Dr. Vivian Argento, executive director of geriatrics and palliative care at Bridgeport Hospital.
When one or both of the strands breaks, DNA repair proteins – including BRCA1 – work to fix the strands so that the cell does not die.
“It’s not surprising if you k now what BRCA does”, Argento said. The findings suggest that DNA restoration in the brain is dampened in patients with Alzheimer’s disease.
To do so, the researchers analyzed neuronal BRCA1 levels in post-mortem Alzheimer’s patient brains, comparing the findings with those taken from healthy tissue.
Also, when they knocked out the BRCA1 gene in parts of the brains of healthy mice, it led to increased breaks in DNA and various neurological impairments.
There is a view that defects in DNA fix may contribute to brain disorders like Alzheimer’s – a disease that causes death of brain cells and is also characterized by build-up of faulty amyloid proteins in and around brain cells.
“By normalising the levels or function of BRCA1, it may be possible to protect neurons from excessive DNA damage and prevent the many detrimental processes it can set in motion”.
The effects are similar in the case of people having Alzheimer’s disease.
It falls to further studies to find out if BRCA1 could be a target for drugs to treat dementia, and whether the BRCA1 mutations that raise cancer risk may also affect the brain.
Alzheimer’s is a degenerative condition affecting some 5.3 million people in the United States alone.
“We continue to focus on our vision of the world without Alzheimer’s”, Walker said.
The study’s first author Dr Elsa Suberbielle, at the Gladstone Institutes, added: ‘BRCA1 has so far been studied primarily in dividing (multiplying) cells and in cancer, which is characterized by abnormal increases in cell numbers.
There are no current treatments to boost proteins from the BRCA1 gene. The Gladstone researchers theorized that the cycle of DNA damage and fix in the brain is actually what facilitates the learning process.
To test this theory, the scientists reduced BRCA1 levels in neurons in laboratory mice.
Researchers think that the protein can play an important role in the disease detection. They introduced amyloid-beta proteins, which are central to Alzheimer’s disease, building up to form harmful plaques in the brain, to neurons grown in cell culture.
They noticed that when they reduced the BRCA1 levels in the brains of health mice, the animals developed problems with learning and memory. In addition, the researchers found reductions of BRCA1 in the brains of mouse models of Alzheimer’s.
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‘This study supports and strengthens that theme by showing that beta-amyloid decreases the level of the DNA fix gene BRCA1, and at the same time inhibits the ability to form new memories’.
