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.

Alzheimer’s disease and Parkinson’s disease are known in the medical world as transmissible spongiform encephalopathy (prion disease).

Prion disease is now the fastest-growing cause of death in the world. The truth is more elusive than a cure. Many factors are contributing to the surge, including misinformation, disinformation and reckless public policies.

The medical term for prion disease is transmissible spongiform encephalopathy, which includes ALS, Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, mad cow disease, chronic wasting disease. The operative word is transmissible. Victims generate a tremendous amount of infectious waste.

The major difference between these forms of neurodegenerative disease is the species under attack and the region of the brain that is under attack. The primary difference between Alzheimer’s disease and Parkinson’s disease, for example, is the region of the brain that is under attack by the pathological protein. 

Despite the smoke and mirrors, the major difference between all of these forms of neurodegenerative disease is the species under attack by infectious prions and the region of the brain that is under attack (first symptom). The primary difference between Alzheimer’s disease and Parkinson’s disease, for example, is the region of the brain that is under attack by the pathological protein. Learn how to prevent and treat all forms of prion disease.

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.

None of the control mice went on to develop Alzheimer’s disease, while 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.

There are proven strategies to help avert neurodegenerative disease, including nutrition, exercise and prion aversion. There is not a cure for prion disease. Preview and order the eBook now to defend yourself and your family.

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