Caregivers At Risk Of Prion Transmission
A study led by led by the University of Texas Medical School at Houston in the US confirms that Alzheimer’s disease is an infectious disease. The researchers injected a small amount of Alzheimer’s disease human brain tissue into the brains of mice bred never to develop this kind of brain alteration, and found the animals gradually developed the disease and that it spread to other parts of the brain.
Alzheimer’s disease is the most common type of prion disease. It affects memory, thinking and behavior, and gets worse with time. The two main hallmarks of the disease are build-up in the brain of misfolded amyloid beta protein, and twisted fibers of tau protein.
In the US there are 5.4 million people with Alzheimer’s disease.
Although there is compelling evidence that build-up of misfolded amyloid beta is a major factor in the disease, we know very little about what might trigger this in otherwise normal proteins, except that in prion diseases like mad cow disease and CJD, the damage is also due to accumulation of misfolded versions of otherwise normal proteins. Prions are infectious misfolded proteins (the word prion comes from the first two letters of protein and the last three of infection).
Senior author Dr Claudio Soto, professor of neurology at The University of Texas Medical School at Houston, said in a statement:
“The underlying mechanism of Alzheimer’s disease is very similar (if not identical) to the prion diseases. It involves a normal protein that becomes misshapen and is able to spread by transforming good proteins to bad ones.”
“The bad proteins accumulate in the brain, forming plaque deposits that are believed to kill neuron cells in Alzheimer’s disease patients,” he added.

For their study, Soto and colleagues injected brain tissue from a confirmed Alzheimer’s patient into mice, which, without exposure to such material, would never develop these alterations.
They also injected a similar amount of brain tissue into a second group of similarly bred mice, except in that group (the controls), the injected tissue came from someone who did not have Alzheimer’s disease.
The results showed that none of the control mice went on to develop signs of Alzheimer’s, while all those injected with Alzheimer’s brain tissue developed plaques and other hallmarks of the disease.
“The accumulation of amyloid beta deposits increased progressively with the time after inoculation, and the [amyloid beta] lesions were observed in brain areas far from the injection site,” write the researchers.
They conclude that these findings suggest some of the typical brain abnormalities seen in Alzheimer’s disease “can be induced by a prion-like mechanism of disease transmission through propagation of protein misfolding.”
This could have broad implications for understanding the underlying mechanisms that trigger Alzheimer’s, and may help develop ways to prevent and treat the disease, they added.
“We are currently working on whether disease transmission can happen in real life under more natural routes of exposure,” said Soto.
Funds from the George P. and Cynthia W. Mitchell Center for Research in Alzheimer’s Disease and Related Brain Disorders at University of Texas Health (UTHealth) helped pay for the study. Soto is director of the Mitchell Center.
Learn more about Dr. Stanley Prusiner and the Nobel Prize for prion science and prion disease.
