Scientists in the United States have identified evidence suggesting that a protein commonly linked to Parkinson’s Disease may contribute to a faster progression of Alzheimer’s Disease in women. The findings, reported by researchers at the Mayo Clinic and published in the journal JAMA Network Open, provide new insights into biological factors that may influence how neurodegenerative diseases develop differently between sexes.

The study examined how the accumulation of the protein alpha-synuclein — widely associated with Parkinson’s disease and related neurological conditions — might interact with pathological processes already present in Alzheimer’s disease.

Interaction between proteins in neurodegenerative diseases

Alzheimer’s disease is primarily characterised by the abnormal accumulation of tau protein in the brain, which disrupts communication between neurons and contributes to progressive cognitive decline. However, researchers note that many individuals diagnosed with Alzheimer’s also develop abnormal deposits of another protein known as alpha-synuclein.

Both tau and alpha-synuclein naturally occur in the human brain. In neurodegenerative conditions, these proteins can misfold and accumulate into abnormal aggregates, damaging nerve cells and interfering with brain function. Scientists have long suspected that when multiple pathological proteins coexist, they may influence how quickly neurological deterioration occurs.

The recent research investigated whether the simultaneous presence of these protein abnormalities alters the course of Alzheimer’s disease and whether the effect differs between women and men.

Findings based on long-term neurological data

To explore this question, researchers analysed information from 415 participants enrolled in the Alzheimer’s Disease Neuroimaging Initiative, a large international research programme that monitors brain changes over time using advanced imaging technologies and biological markers.

Participants underwent cerebrospinal fluid testing to detect abnormal alpha-synuclein levels and repeated neuroimaging scans to measure the accumulation of tau protein in the brain. Approximately 17 per cent of the participants showed evidence of abnormal alpha-synuclein.

Among individuals who displayed both Alzheimer’s-related pathology and alpha-synuclein abnormalities, women experienced a markedly faster increase in tau accumulation compared with men with similar biological markers.

Understanding gender differences in dementia risk

The findings may help explain a long-recognised epidemiological pattern: women represent nearly two-thirds of people living with Alzheimer’s disease worldwide. Researchers involved in the study emphasise that identifying sex-specific biological mechanisms could support the development of more targeted clinical trials and personalised treatment strategies.

Specialists in neuroimaging involved in the research have highlighted the importance of recognising that Alzheimer’s disease may not progress in exactly the same way for all patients. Coexisting brain pathologies, such as those associated with Parkinson’s disease, may influence how quickly symptoms develop.

Implications for future research

Experts believe the results open new avenues for investigating why women appear to be disproportionately affected by certain forms of dementia. Understanding how different proteins interact in the brain may help scientists identify previously overlooked therapeutic targets.

Researchers are now examining whether similar sex-specific patterns occur in other neurological conditions involving alpha-synuclein, including Lewy Body Dementia. These studies aim to determine whether the observed vulnerability is unique to Alzheimer’s disease or reflects broader biological differences across multiple neurodegenerative disorders.

As global populations age, improving understanding of the biological mechanisms underlying dementia has become a major priority for medical research. Studies conducted in the United States and other countries continue to highlight the complex interplay between genetic, molecular and demographic factors that shape the progression of neurological disease.