Brain protein offers clues about higher risk in older women



A new study recently discovered that women who died from Alzheimer’s had a higher amount of a chemically-modified version of the protein complement C3 in their brains compared to men who died from the disease.

The researchers believe the drop in estrogen caused by menopause may leave women more vulnerable to this version of complement C3.

Although anyone can develop Alzheimer’s disease (AD), a type of dementia associated with cognitive decline and memory loss, previous research has shown that females are more likelyTrusted Source to have the condition than men.

In fact, in the United States, almost two-thirds of Alzheimer’s cases are women.

Now, a recent study from scientists at Scripps Research and Massachusetts Institute of Technology (MIT) has uncovered a new clue as to why women may be at a higher risk for Alzheimer’s. The findings point to an inflammatory immune protein called complement C3.

Researchers found a much higher level of a chemically-modified version of the C3 protein in the brains of women who died from Alzheimer’s compared to men who also died from the disease.

Additionally, the research team showed the hormone estrogen normally helps protect against this chemical modification of complement C3. But estrogen levels typically decline in women during menopause.

The study was recently published in the journal Science Advances.

What is complement C3 protein?

According to Dr. Stuart Lipton, Ph.D., professor and Step Family Foundation Endowed Chair in the Department of Molecular Medicine at Scripps Research, a clinical neurologist in La Jolla, CA, and senior author of this study, complement C3Trusted Source is a component of a cascade of proteins in the blood that mediate inflammatory infections, usually to fight infections.

“However, they are also known during development to help sculpt new synapsesTrusted Source, the connections between nerve cellsTrusted Source that allow them to talk to one another and are the basis for learning and memory,” he told Medical News Today. “In disease, excessive activity of complement C3, however, can result in loss of synapses, contributing to dementia.”