In 2007, James Watson eyed his genome for the very first time. Through more than 50 years of scientific and technological advancement, Watson saw the chemical structure he once helped unravel now fused into a personal genetic landscape laid out before him.
Yet there was a small stretch of nucleic acids on chromosome 19 that he preferred to leave uncovered, a region that coded the apolipoprotein E gene. APOE, as it’s called, has been a telling genetic landmark of Alzheimer’s risk, strongly correlated to the disease since the early 90s. Watson’s grandmother suffered from Alzheimer’s, and without any reasonable treatments or suitable preventive strategies, the father of DNA decided the information was too volatile, its revelation creating more potential harm than good.
Watson’s apprehension was warranted. Treatments for Alzheimer’s Disease have consistently failed, sometimes miserably. But as we learn more and more about the brain, it has become apparent that genetics alone rarely dictate the course of disease. Instead, brain disorders result from a complex interaction of our genes and the environments to which we’re exposed. And now, a recent wave of research has unveiled another player in the genesis of neurodegenerative disease: stress.
While scientists have already catalogued the effect of our surroundings and environment on psychological conditions – including depression and anxiety disorders – new studies suggest that stress may also figure into the complex equation that determines if someone will develop a neurodegenerative disease or not. Because stress can be mitigated through lifestyle changes, people may finally gain some control over these devastating, and feared, illnesses.
Since Alois Alzheimer first noted his clinical findings of “presenile dementia” in a patient at the turn of the twentieth century, doctors have continually observed that the disease tends to run through families. But it wasn’t until the early 90s, when a team led by Margaret Pericak-Vance, then a researcher at Duke University Medical School, uncovered the genetic link to Alzheimer’s Disease. By extracting DNA from circulating lymphoblasts, Pericak-Vance and colleagues were able to correlate Alzheimer’s Disease to variations of the APOE gene on chromosome 19.
Around the same time, another group of researchers at Duke University’s Department of Psychiatry and Behavioral Science, led by Brenda Plassman, started a series of experiments to see if non-genetic factors contributed to Alzheimer’s. They wondered: could a person’s environment also affect whether or not they’d acquire the disease?