It was discovered in 1906 by its namesake, Dr. Alois Alzheimer. But it wasn’t until the 1980s that research on causes and prevention began, so it’s only been studied for the past 40 years, making the research field comparably young compared to other conditions like heart disease and cancers.
But two researchers are turning what we thought we knew about Alzheimer’s on its head.
Here’s how: Beta-amyloid, a sticky protein that clumps together and kills brain cells leading to cognitive decline, has been heralded as what we need to understand to cure the disease, according to Alzheimer’s Association. Researchers have been studying ways to find genetic mutations linked with beta-amyloid production or drugs to target the protein before it causes too much damage.
Since 2010, Tanzi and Moir, have shown that amyloid-beta, a protein linked to Alzheimer’s, is actually antimicrobial, meaning it’s developing in the brain by fighting against something.
“We assumed that amyloid-beta protein in the plaque is just an abnormality that happens with age, but over the last 10 years, Rob and I discovered that the amyloid-beta protein actually plays a role in the brain by protecting the brain against infection,” Tanzi said.
This just so happens to connect with the body’s ancient immune system.
“Turns out, our most ancient immune system, before we had adaptive immunity, had little baby proteins, antimicrobial peptides, and when they saw bacteria or a virus or a fungus, they would stick to it and clump it up into a ball and the peptide would grow into a spiral like spaghetti and trap it like a fly trapping a seed, and that is one of the most classic ways that our primitive innate immune system protects us,” he said.
One of these known peptides is called LL-37, which Moir and Tanzi discovered was molecularly similar to the amyloid-beta protein. Moir and Tanzi started with a petri dish, putting Alzheimer’s genes in it and adding a microbe to the dish. Amyloid-beta plaques built up overnight.