THE HILL - Scientists in California tried to study Alzheimer’s disease from a different perspective and the results may have led them to the cause of the disease.
Researchers at the University of California- Riverside (UCR) recently published results from a study that looked at a protein called tau. By studying the different forms tau proteins take, researchers discovered the difference between people who developed dementia and those who didn’t.
The tau protein was critical for researchers because they wanted to understand what the protein could reveal about the mechanism behind plaques and tangles, two critical indicators doctors look for when diagnosing people with Alzheimer’s.
By analyzing donated brain samples, researchers found that those with brain buildup, like plaques and tangles, but had no dementia had a normal form of tau. However, those who had a “different-handed” form of tau and developed plaques or tangles did have dementia.
Ryan Julian, a chemistry professor at UCR, said in a press release, “roughly 20% of people have the plaques, but no signs of dementia. This makes it seem as though the plaques themselves are not the cause.”
The amino acids that make up proteins like tau can either be right-handed or left-handed isomers, and normally proteins in living things are made from all left-handed amino acids, explained Julian.
However, most proteins only survive for less than 48 hours in the body, and if they hang around too long, certain amino acids can convert into the other-handed isomer. So that means a left-handed isomer could inadvertently convert into a right-handed isomer, which can lead to serious problems.
“If you try to put a right-handed glove on your left hand, it doesn’t work too well. It’s a similar problem in biology; molecules don’t work the way they’re supposed to after a while because a left-handed glove can actually convert into a right-handed glove that doesn’t fit,” said Julian.
However, the human body has a solution through a process called autophagy, which clears spent or defective proteins from cells.
Unfortunately, as people age autophagy slows down, especially in people over the age of 65. It’s not clear exactly why, and Julian’s lab intends to study the phenomenon.
Fortunately, there are drugs currently being tested to improve the process of autophagy, and some existing ones that are approved for cardiovascular disease and other conditions could speed up the approval process
According to UCR, autophagy can be induced by fasting because when cells run short on proteins from a person’s diet, they fill the void by recycling proteins already present in cells. Exercise is also another way researchers say can increase autophagy.
If there is a connection between autophagy and developing Alzheimer’s, Julian said, “if a slowdown in autophagy is the underlying cause, things that increase it should have the beneficial, opposite effect.”