In the largest related finding to date, researchers in two independent studies have identified a total of three genetic immune-system risk factors for Alzheimer's disease. These studies estimate that the identified elements account for 20% of AD's genetic origins. One of them is perhaps the strongest single link tested to date. In addition to these findings, a third study has drawn a stronger link between AD and inflammation in the vascular system.

 

While the data gathered in these studies means little to the layman, they will profoundly alter the course of AD research. The most significant aspect of this work is the fact that two independent studies identified the same gene for the first time. Hundreds of possible Alzheimer's genes have been proposed, and though all may well be related in some cases, none have passed the independent confirmation test. This gene, known as APOE, works to create beta amyloid, the substance that makes up the white plaque found in the brain cavities of advanced AD subjects. The other genes uncovered by these studies are clusterin, responsible for clearing rogue proteins from the brain cavity, and CR1, another step in a long chain of chemical reactions intended to remove toxins from the body.

 

A third study focussed on a protective substance (called TNF or tumor necrosis factor alpha) released by white blood cells to combat inflammation, or excessive swelling in the bloodstream. In keeping with earlier experiments on mice, the subjects whose bodies bore the highest levels of TNF at the beginning of this study were nearly four times as likely to display symptoms of significant cognitive decline by its end. Researchers believe that these substances, intended to destroy dead or infected tissues, may overreact to inflammation and kill healthy brain cells as well, facilitating common difficulties with memory and coherence. The fact that all three studies tied Alzheimer's risks to immune system's ability to repair itself is a significant development. Susceptible subjects may carry these genetic variations that comprise the body's powers of self-preservation.

 

The most significant immediate effect of this research may be a renewed focus on cardiovascular health as an Alzheimer's preventative. Avoiding inflammation and heart disease by maintaining a physically active lifestyle may well be more central to the AD equation than previously thought. Treatment plans drawn from the results of these studies are, unfortunately, still a long way off. But the research community is slowly drawing closer to AD's underlying biology, and these announcements mark a big step forward.