Alzheimer’s is one of the most common forms of dementia among the elderly and it is estimated that approximately 1 in 10 people over 65 years of age suffers from it .
Although there is no treatment to cure it, a group of researchers at the University of Washington has detected a new compound that protects against brain damage produced by an Alzheimer’s protein .
The tests show how this compound directly targets the APOE protein. Among its different variables, APOE4 is the main genetic risk factor for the development of the disease . In fact, between 60 and 80% of those with Alzheimer’s have at least one allele of these characteristics.
“Scientists have been interested in APOE for years, but there are only a few examples where researchers have approached it with a compound in live animals,” says one of the authors of the discovery, David Holtzman .
The so-called ‘ beta amyloid ‘ is an adhesive protein that creates plaques in the brain. These plaques appear in Alzheimer’s patients years before characteristic symptoms such as memory loss or confusion become visible in the affected person.
In this way, APOE4 has been shown to increase the risk of Alzheimer’s , in part, by stimulating the accumulation of beta amyloid in harmful plaques . According to the figures, carriers of this protein have up to 12 times the risk of developing Alzheimer’s than the rest of the population.
Road to royal treatment
The research focused on studying those mice genetically prone to developing amyloid plaques in their brains and carrying the human genetic variant APOE4 .
The first tests were with newborn rodents . These were divided into two groups: those who had been injected into the fluid surrounding the brain with the compound APOE, and those who had been given a placebo.
Levels of the protein dropped by half in mice that had received APOE compared to those that had not.
It was later tested whether administering APOE after the appearance of amyloid plaques could prevent further changes in the brain. This time, the tests were done on the brains of older mice .
They found no difference in the number of plaques or the total amount of beta amyloid between the mice that received the compound and those that received only the placebo. The compound failed to reduce the amount of amyloid in the brains of the mice.
However, in APOE-treated mice, each plaque triggered only half the damage to surrounding neurons , suggesting that even a late start could reduce the damage caused by beta amyloid.
According to Holtzman “our findings indicate that APOE is not only involved in Alzheimer’s risk and disease progression, but could also be a real target for treatment or prevention “
Clusters of a harmful Alzheimer’s protein (white spots) are rarer in the brains of mice treated with the compound (top) compared to those given a placebo (bottom).
