Scientists at Northwestern University have discovered new clues into the chain of events that causes Alzheimer’s. As this ScienCentral News video reports, they wanted to settle the debate about plaques that form in the brain.
John Disterhoft, physiology professor at the Feinberg School of Medicine at Northwestern, studied this in mice. Disterhoft and his team genetically altered a strain of mice so that they would be prone to get Alzheimer's. They did this by giving the mice a human gene that causes excess formation of amyloid precursor protein, or APP.
A mouse in a Y maze
As the mice got older, they were found to have a greater amount of beta-amyloid protein, a small, sticky protein fragment that tends to clump together, in their brains. They were also less able to remember their cage mates, and they got lost in a simple three-armed maze called a Y-maze. "[This] kind of learning is similar to the kind of learning that individuals with Alzheimer's disease have problems with," says Disterhoft. "They have trouble remembering."
But when the team eliminated an enzyme, called beta-site APP cleaving enzyme 1, or BACE1, which helps to make the beta-amyloid protein, the nerve cells in the brains of the mice stayed healthy, and they didn't get lost.
Disterhoft says this indicates that even before plaques in the brain are actually formed, beta amyloid floating in the brain is capable of causing the learning defects and changes in cellular responses that represent Alzheimer's disease.
"What our study indicates is, [it's] not plaques that causes Alzheimer's disease but rather the beta-amyloid that is the pre-curser, or is thought to be the pre-curser, of plaques is actually what is toxic to the brain and causes behavioral and physiological deficits that are associated with Alzheimer's disease once it's already developed," says Disterhoft. "We have clearly shown that if we eliminate formation of beta amyloid in the brain of these mice, they do not develop the learning defects and the alterations in cellular excitability that are seen in the Alzheimer's model."
If the study is confirmed, it would indicate that beta-amyloid buildup is probably a major cause of Alzheimer's and that future drug treatments would aim to block that buildup, perhaps by getting rid of the BACE1 enzyme. There are drugs that can get rid of the enzyme, but further tests are needed to see how they'll work on humans.
One in 10 people over 65 and nearly half of those over 85 have Alzheimer’s disease. The United States spends at least $100 billion a year on the disease, and neither Medicare nor most private health insurance covers the long-term care most patients need.
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