Two of the most common and dreaded illnesses in America may share a connection, with new research suggesting that having insulin resistance or type 2 diabetes raises your risk of developing the brain plaques associated with Alzheimer's disease.
After adjusting for other risk factors, the Japanese study found that people with the highest levels of fasting insulin had nearly six times the odds of having plaque deposits between nerves in the brain, compared to people with the lowest levels of fasting insulin.
When Henry McCance started at Greylock Partners in 1969, the venture capital industry had less than $100 million flowing into it each year, he estimates. Now, it's roughly a $20 billiion-a-year sector of the financial world that has backed companies whose products are, in many cases, staples of modern living.
Five years ago, McCance, now Greylock's chairman emeritus, started a nonprofit research foundation called the Cure Alzheimer's Fund.
Many doctors already suspect there may be a link between surgery and the onset of Alzheimer's.
Previous studies have suggested that between 10 and 30 percent of elderly people who undergo surgery suffer memory problems afterwards, but it has not been established whether these are a short-term response to physical trauma, or the beginnings of dementia.
Cognitive problems, ranging from memory loss to delirium, have been found most commonly when elderly people have undergone heart surgery, but also following other operations.
In 2003, a group of scientists and executives from the National Institutes of Health, the Food and Drug Administration, the drug and medical-imaging industries, universities and nonprofit groups joined in a project that experts say had no precedent: a collaborative effort to find the biological markers that show the progression of Alzheimer's disease in the human brain.
The scene was a kind of science court. On trial was the question “Can anything - running on a treadmill, eating more spinach, learning Arabic - prevent Alzheimer's disease or delay its progression?”
To try to answer that question, the National Institutes of Health sponsored the court, appointing a jury of 15 medical scientists with no vested interests in Alzheimer’s research. They would hear the evidence and reach a judgment on what the data showed.
Will Alzheimer's disease, a terrible degenerative brain disease with no treatments and no clear guidelines for diagnosis before its end stages, become like heart disease? Will there be early markers of risk, analogous to high cholesterol levels, that will predict who is likely to get it? And will there be drugs that actually prevent it?
In 1966, as a visiting medical student at a London teaching hospital, I interviewed a husband and wife, in their early twenties, who had recently experienced a truly calamitous health catastrophe. On their wedding night, in their first experience of sexual intercourse, a malformed blood vessel in the husband's brain burst, leaving him with a disabling paralysis of the right side of his body. Stunned and guilt-ridden, the couple clutched hands and cried silently as they shared their suffering with me.
Harvard researchers have uncovered a mechanism through which caloric restriction and exercise delay some of the debilitating effects of aging by rejuvenating the connections between nerves and the muscles that they control.
The research, conducted in the labs of Joshua Sanes and Jeff Lichtman, both members of the Center for Brain Science at Harvard and professors of molecular and cellular biology, begins to explain prior findings that exercise and restricted-calorie diets help to starve off the mental and physical degeneration of aging.