New animal research suggests the brain damage caused by Alzheimer’s disease may result from an infectious process similar to “mad cow” disease.
Investigators from The University of Texas Health Science Center at Houston believe brain damage that characterizes Alzheimer’s disease could originate in a form similar to that of infectious prion diseases (such as bovine spongiform encephalopathy and Creutzfeldt-Jakob).
“Our findings open the possibility that some of the sporadic Alzheimer’s cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease,” said researcher Claudio Soto, Ph.D.
“The underlying mechanism of Alzheimer’s disease is very similar 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.”
The results showing a potentially infectious spreading of Alzheimer’s disease in animal models were published in the online issue of Molecular Psychiatry, part of the Nature Publishing Group.
In Alzheimer’s disease, brain plaques are hallmarks of the illness and are caused by misshapen aggregates of beta amyloid protein and twisted fibers of the protein tau.
In the study, researchers injected the brain tissue of a confirmed Alzheimer’s patient into mice and compared the results to those from injected tissue of a control without the disease.
None of the mice injected with the control showed signs of Alzheimer’s, whereas all of those injected with Alzheimer’s brain extracts developed plaques and other brain alterations typical of the disease.
“We took a normal mouse model that spontaneously does not develop any brain damage and injected a small amount of Alzheimer’s human brain tissue into the animal’s brain,” said Soto.
“The mouse developed Alzheimer’s over time and it spread to other portions of the brain. We are currently working on whether disease transmission can happen in real life under more natural routes of exposure.”