What causes Alzheimer's disease remains a mystery to scientists and doctors.
But a recent experiment in mice suggests that the layering of beta amyloid deposited in neurons, a key sign of Alzheimer's, can be recreated in animals. The study opens the door to the possibility that Alzheimer's might spread in a similar way to other illnesses caused by prions, such as bovine spongiform encephalopathy (Mad Cow disease) and Creutzfeldt-Jakob disease. So far, prions are also known to cause the fatal neurological condition Kuru in humans and chronic wasting disease in deer, among others.
Prions can destroy brain tissue by creating misshapen proteins. These bits of infectious material, different from bacteria and viruses, cause proteins to fold abnormally, similar to what happens to amyloid in the brains of Alzheimer's patients and individuals with other conditions, including Parkinson's and Huntington's.
Discovery Fit & Health: Alzheimer's Overview
Amyloids, or small snippets of proteins, are produced regularly by the brain but are broken down. But for people with Alzheimer's, amyloids fold abnormally and form plaque in the brain, like plaque buidup on teeth, which appear to produce negative effects. In this light, amyloids aren't always harmful, but they can be when they build up.
This is where the mice come in. Scientists injected brain material from a deceased person with Alzheimer's into the brains of live mice. As a control, they did the same with a much younger, non-diseased brain, too. The mice have the same proteins that are affected by Alzheimer's, but do not naturally show the amyloid plaque deposits characteristic of the disease. Mice were euthanized after 30, 90, 285, 450 and 585 days following the injection, so researchers could study their brains.
They found that the injections from the diseased brain caused proteins to "misfold" in the mice's brains much like what happens during Alzheimer's. Even more, the amyloid deposits increased over time and appeared in areas of the brain that weren't close to the injection site. Ultimately, this suggests amyloid deposits unique to Alzheimer's might be "induced by a prion-like mechanism of disease transmission," the authors write.
Here, abnormal protein folding and its ability to spread by injecting infected tissue resembles prion infections. This isn't to say prions cause Alzheimer's, but it suggests the two seem to work in similar ways, which gives scientists more leads on how to tackle the disease.
Previous research hints at a link between Alzheimer's and prion proteins, suggesting that more proteins equate to fewer cases of amyloid buildup.
Despite the findings, it's likely other well-researched factors, including family history, genetics and a person's lifestyle, shape the onset of the disease as well.
Alzheimer's is a fatal disease that affects a person's memory, personality and thinking.