Researchers at the Gladstone Institute of Neurological Disease have discovered an interesting link between the BRCA1 gene and Alzheimer’s.
Scientists have long known how the BRCA gene can increase the risk of a person developing breast and ovarian cancers, but little research has been conducted into how the gene can influence other degenerative diseases in the body.
Published in the journal Nature Communications, a study conducted by Lennart Mucke, Director of the Gladstone Institute, found that aside from affecting cellular growth of cancer, it can also inhibit the repair function of nerve cells.
The strange thing researchers learnt about the gene was that it can mutate itself in different ways. While at particular stages it manifests itself as fuel, aiding in the growth of cancerous tumours, it can also be responsible for repairing DNA in some cases.
When analysing the autopsy results of humans who had died with Alzheimer’s, their brains had levels of BRCA1 that were 75% lower, than those who had died with no Alzheimer’s present.
What this shows, according to researchers, was that the accumulation of the amyloid protein, a notable part of Alzheimer’s, could intensify the depletion of BRCA.
“We think amyloid probably comes first. That depletes BRCA1 and that then leads to the accumulation of DNA damage because they aren’t repaired properly. That very likely has an impact on the expression of many genes involved in learning and memory,” according to Lennart Mucke.
The experiments that followed mice who carried the BRCA1 gene found that the same protein was a vital ingredient in ongoing brain health.
When the mice showed low levels of the protein, their cellular function and level of renewal, diminished.
Whilst the results are only in the initial stages of testing, further studies will be conducted to pursue implications of these newly discovered link.
Studies will now be conducted into how anti-amyloid drugs could be helpful in those who have the BRCA1 mutation by assisting in reducing the development of Alzheimer’s. Similarly, investigations will begin into whether women who develop BRCA1 mutations later in life, could be at a heightened risk of Alzheimer’s also.
“Therapeutic manipulation of repair factors such as BRCA1 may ultimately be used to prevent neuronal damage and cognitive decline in patients with Alzheimer’s disease or in people at risk for the disease.
“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.”
“According to our study, deficits in DNA repair seem to contribute to the cognitive decline of Alzheimer’s disease,” says Mucke. “That becomes an interesting strategy for potentially improving DNA repair as a way to treat the disease, something that has not yet been widely pursued.”