Alzheimer’s disease is a hereditary condition. About 60% of the risk for the degenerative brain disease is thought to be genetic, based on the results of twin studies. The best known evidence of this is a gene called apolipoprotein E. People with a variant called APOE e4 are more likely to develop Alzheimer’s. But what accounts for the rest of the risk?
A study published in today’s edition of Archives of General Psychiatry helps fill in those gaps.
A team of Dutch researchers compared 206 middle-aged adults whose parents had late-onset Alzheimer’s to another group of 200 similarly aged adults with no parental history of the disease. They found that both groups had much in common, including levels of smoking, physical activity and intake of dietary fat. But there were significant differences in various measurements of blood pressure and inflammation.
For instance, the children of Alzheimer’s patients had higher systolic and diastolic blood pressure, and 40% of them had hypertension, compared with 29% of those in the control group. The Alzheimer’s offspring also had a lower ankle brachial index -- a comparison of resting blood pressure in the ankle and arm that is a sign of peripheral artery disease.
The researchers tested blood samples from both groups and found that the children of Alzheimer’s patients had significantly higher levels of several kinds of proinflammatory cytokines. Since these markers typically circulate at very low levels, the researchers said they are probably a consequence of the disease rather than a cause.
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