High blood pressure, evidence of arterial disease and markers of inflammation in the blood in middle age appear more common in individuals whose parents have Alzheimer’s disease than in individuals without a parental history of the condition, according to a new report.

The report followed at study by doctors who compared some of these vascular and inflammatory factors, such as high blood pressure and levels of cytokines between 206 offspring of 92 families with a history of Alzheimer’s disease and 200 offspring of 97 families without a parental history.

Researchers measured blood pressure; obtained blood samples to assess genetic characteristics and levels of cholesterol, along with cytokines and other inflammation-related substances; and collected sociodemographic characteristics, medical history and information about diet, exercise and stress levels. More individuals whose parents had Alzheimer’s disease carried the APOE ε4 gene, known to be associated with the condition, than did those with no family history (47 per cent v 21 per cent).

In addition, those with a family history had higher systolic and diastolic blood pressures, a lower ankle brachial index and higher levels of several different pro-inflammatory cytokines.

Other cardiovascular risk factors – such as high blood cholesterol and glucose levels – were not associated with parental Alzheimer’s disease. These other components may not be as closely linked to cognitive decline, the study’s authors wrote.

“Our study shows that high blood pressure and an innate pro-inflammatory cytokine response in middle age significantly contribute to Alzheimer’s disease,” they continued. “As these risk factors cluster in families, it is important to realize that early interventions could prevent late-onset Alzheimer’s disease. One could argue for a high-risk prevention strategy by identifying the offspring of patients with Alzheimer’s disease, screening them for hypertension and vascular factors and implementing various (non)pharmacological health measures.”

Archives of General Psychiatry 2009;66:1263-1270