While having the ApoE4 gene is a major genetic risk factor for Alzheimer’s disease (AD), not all ApoE4 carriers develop the disease. But new research shows that ApoE4 coupled with chronic inflammation dramatically increases the risk of AD.
This can be detected by sequential measurements of C-reactive protein, a common clinical test that can be could be done routinely in a clinical setting, according to researchers at Boston University School of Medicine (BUSM).
“Finding out what mediating factors for ApoE4 increase AD risk is important for developing intervention and prevention of the disease,” said corresponding author Wendy Qiu, M.D., Ph.D., an associate professor of psychiatry and pharmacology and experimental therapeutics at BUSM.
“Since many elders have chronic low-grade inflammation after suffering from common diseases like cardiovascular diseases, diabetes, pneumonia, and urinary tract infection, or after having surgeries, rigorously treating chronic systemic inflammation in ApoE4 carriers could be effective for prevention of Alzheimer’s dementia.”
Using data from the Framingham Heart Study, which includes more than 3,000 subjects, the researchers studied patients with the ApoE4 gene and those with and without chronic low-grade inflammation defined by sequential C-reactive protein measurements.
They found ApoE4 with chronic low-grade inflammation was more strongly related to the onset of dementia, as well as AD, compared to ApoE4 carriers without inflammation.
Qiu said she believes that without chronic low-grade inflammation, there could be no difference of Alzheimer’s risk between ApoE4 and non-ApoE4 carriers, adding anti-inflammatory treatments could be effective for AD prevention.
The study was published in JAMA Network Open.