Vascular risk factors at midlife, such as diabetes and smoking, may play a key role in the development of Alzheimer's disease. A study has suggested that they contribute to amyloid plaque deposition – a hallmark of the disease.
Researchers had already established that major vascular risk factors identified at midlife are associated with a higher risk of late-life dementia, but results had at time been inconsistent.
Furthermore, it wasn't clear whether these factors were directly involved in causing the neurodegeneration specifically associated with Alzheimer's disease – such as the deposition of amyloid plaques – and if they lead to other cerebral changes.
"Other studies have suggested an association between midlife vascular risk factors and dementia or even Alzheimer's disease, but we didn't have a clear understanding before of whether amyloid itself, is directly impacted by vascular risk", study lead author Rebecca Gottesman told IBTimes UK.
The complete findings are now published in the journal JAMA.
Midlife vs. late life
The team from John Hopkins School of Medicine (US) analysed the data of 346 participants from a large prospective cohort study in the US.
All had been regularly evaluated for vascular risk factors and markers since 1987-1989 after entering the study at midlife (between the age of 45 and 64). Between 2011 and 2013, they went through PET scans which allowed for the detection of amyloid plaques in their brains.
The vascular risk factors examined in the study included diabetes and smoking, but also hypertension, high body mass index and high levels of cholesterol in the blood.
The scientists found that people who had two or more of these vascular risk factors at midlife were significantly more at risk of having elevated amyloid deposition in the brain later in life, compared with those who had none.
However, late-life vascular risk factors were not associated with late-life brain amyloid deposition.
These findings are consistent with the idea that vascular disease may play a role in the development of Alzheimer's disease, by increasing the amount of amyloid plaques present in the brain later in life.
Gottesman concluded: "The risk factors we identified are all modifiable, but we otherwise don't have a way to prevent or treat Alzheimer's disease. Our study doesn't directly show that treating these risk factors would reduce the risk of Alzheimer's disease, but it still seems that this may be an opportunity to potentially reduce Alzheimer's risk".