Study: Male Brains Age Faster, Yet Women Face Higher Alzheimer's Risk
Male brains age faster, but women have higher Alzheimer's risk

A groundbreaking new study has turned conventional wisdom on its head, revealing that men's brains may age faster than women's. This finding complicates the long-standing medical puzzle of why women face a significantly higher risk of developing Alzheimer's disease.

Tracking Brain Changes Over Time

The international research, led by neuroscientists at the University of Oslo and published in the journal Proceedings of the National Academy of Sciences, analysed data from over 4,700 healthy adults aged between 17 and 95. None of the participants had Alzheimer's or any cognitive impairment.

Each volunteer underwent at least two MRI scans over an average follow-up period of three years. This allowed scientists to meticulously track subtle changes in brain structure, including volume loss and cortical thinning, over time.

The results were striking. Male brains showed a greater reduction in volume and signs of decline in more regions compared to female brains. A key area of difference was the postcentral cortex, responsible for processing touch and body awareness. This region declined by an average of 2% per year in men, compared to just 1.2% per year in women.

Men also exhibited more pronounced thinning in regions linked to visual processing, memory, learning, and movement. While women did show some signs of faster decline—such as a quicker expansion of fluid-filled brain ventricles—the researchers concluded that, overall, male brains appeared to age more rapidly.

Rethinking the Alzheimer's Risk Paradox

These findings directly challenge a popular theory that sought to explain women's elevated Alzheimer's risk. For years, scientists have tried to understand why women are almost twice as likely to develop the most common form of dementia. One hypothesis was that women's brains might age faster, making them more vulnerable.

Professor Charles Marshall, a clinical neurologist at Queen Mary University of London who was not involved in the study, told BBC Science Focus that the research offers strong evidence against this explanation. He clarified the complex link, explaining that Alzheimer's develops from the accumulation of proteins like amyloid and tau. The rate of general brain ageing affects how quickly symptoms appear once these proteins are present.

Alternative Explanations and Future Research

Experts caution that the study is not the final word. Dr. Jacqui Hanley of Alzheimer's Research UK noted important limitations, including the short study period compared to the decades-long development of dementia and the fact that all participants were healthy. Future studies need longer monitoring to see if these observed changes actually lead to Alzheimer's.

Other research points to different mechanisms. A recent mouse study from the University of California, Los Angeles (UCLA) highlighted a gene called Kdm6a, located on the X chromosome. This gene may drive inflammation in brain immune cells. Since women have two X chromosomes, they carry two copies of this gene.

Lead author Professor Rhonda Voskuhl suggested that heightened inflammation might be beneficial earlier in life for fighting infection, with oestrogen keeping it in check. After menopause, falling oestrogen levels could unleash the pro-inflammatory effects of Kdm6a, potentially increasing neurodegeneration. This theory is supported by findings that earlier menopause is linked to higher dementia risk, while hormone replacement therapy is associated with lower risk.

Voskuhl proposed that a two-pronged therapeutic approach—countering inflammation and addressing hormone loss—might be an ideal future solution for women.

For now, the reasons behind women's disproportionate Alzheimer's burden remain an unresolved, complex puzzle. However, this new research, published in December 2025, firmly suggests that faster general brain ageing in women is unlikely to be the primary explanation, adding a crucial and surprising layer to our understanding of dementia.