A new study found that a gene associated with ovarian and breast cancers plays a key role in the formation of Alzheimer's disease. In a lab mice experiemnt, the gene called BRCA1 was found to help in the restoration of broken DNA strands. However, mutated BRCA1 gene is linked to both ovarian and breast cancers.
Researchers from the Gladstone Institutes discovered that people who had cognitive degeneration or died from Alzheimer's had low counts of the BRCA1 gene. Autopsies of Alzheimer's patients and those with mild cognitive decline revealed low BRCA1 levels in the brain. The low count is also linked to the amyloid beta build-up. Amyloid beta is a key part in the plaque that affects the brains of Alzheimer's patients.
The team led by Gladstone Institute of Neurological Disease director Dr. Lennart Mucke reproduced mice with BRCA1 genes, capable of various mutations. They found that in the presence of breast cancer, the BRCA1 gene increases tumor growths. Ironically, the gene also restores damaged DNA. In mice with low BRCA1 counts, DNA repair failed to kick in which led to cognitive problems.
"It is extremely interesting that one molecule can be critically involved in two apparently opposing conditions: cancer, in which too many cells are born and neurodegenerative disease, in which too many brain cells die off," said Mucke.
In the UK, approximately 850,000 people are affected by dementia which costs around £26 billion (over $39 billion) in annual treatments. Currently, there is no treatment aimed at boosting the proteins from BRCA1. However, the Gladstone Institutes are analyzing if memory loss or cognitive decline can be prevented by an increase in BRCA1 levels.
Alzheimer's Research UK's Dr. Simon Ridley expressed that cells are capable of repairing damaged DNA accurately and swiftly. When the innate mechanisms go wrong, the cells are damaged, such as in the case of patients with cancers and other diseases. The findings suggest that DNA restoration in the brain is dampened in patients with Alzheimer's disease. However, further studies are needed to conclude if increasing the cell's ability to repair DNA could relieve the symptoms of dementia.
The study was published in the Nature Communications journal on Nov. 30.
