07 December 2015
ByAppeared in BioNews 831
They found that levels of the normal BRCA1 protein were up to 75 percent lower in the brains of people who died from Alzheimer's disease than in the brains of people who died from other causes.
'It's 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 Professor Lennart Mucke of the University of California, San Fransisco, who conducted the study, which was published in Nature Communications.
BRCA1 is one of several proteins that are important for repairing 'double-strand breaks' in the DNA of healthy brains. This DNA-repair role is vital because, if the breaks aren't repaired, the affected brain cells could die.
The researchers also looked at the brains of mice. They lowered BRCA1 levels in the dentate gyrus, a part of the brain that is affected early in the course of Alzheimer's disease. They found that this BRCA1 reduction caused the cells in this region to become damaged, and these mice had problems with tasks involving learning and memory.
Beta-amyloid is a protein that has long been implicated in Alzheimer's disease, and abnormal accumulations are known to kill neurons in the brain. When the researchers added this protein to a dish containing neurons, they observed that BRCA1 levels were reduced.
Taken together, these findings imply that 'beta-amyloid decreases the levels of the DNA-repair gene BRCA1, and at the same time inhibits the ability to form new memories', according to Dr Roderick Corriveau, program director of the NIH's National Institute of Neurological Disorders and Stroke, who was not involved in the study.