The idea that Alzheimer’s disease could be an infectious disease seems a strange notion. However, over the last decades, there have been occasional reports that in rare occasions people can get ‘infected’ with Alzheimer’s disease. Two international expert groups decided therefore to review the evidence whether Alzheimer’s disease can be infectious and have now published their findings*.
When talking about infection in the context of Alzheimer’s disease we need to understand that we are not talking about infecting someone by simply being in the same room with same or sneezing or coughing in their presence. We can put our mind at ease that we cannot ‘catch’ Alzheimer’s disease like that. Instead, we are talking about infection by blood transfusion or brain tissue transplantation.
What is the mechanism that Alzheimer’s disease is potentially infectious?
The reason for this lies in the proteins which cause Alzheimer’s disease – amyloid and tau. It is the accumulation of amyloid and tau which causes Alzheimer’s disease. However, they not only accumulate in the brain but also ‘spread’ to adjacent areas of the brain. This means that amyloid and tau accumulation starts in one part of the brain, most often in the medial temporal lobe of our brain which is important for our memory and orientation. After amyloid and tau have accumulated in the medial temporal lobes they ‘spread’ to other areas of the brain, until they have accumulated all over the brain in the late stages of Alzheimer’s disease.
The accumulation of amyloid and tau, as well as their spread through their brain, has been known for a long time. However, the mechanism of how amyloid and tau spread throughout the brain is not yet fully understood and still being investigated.
One explanation of why amyloid and tau are spreading through the brain is that they ‘infect’ neighbouring brain cells and areas, which ultimately leads to the disease spreading through the whole brain. For now, this is mostly a theory by scientists, with only limited scientific evidence that such infection takes place. However, if that is the case it would have significant implications, as amyloid and tau would have then ‘prion-like’ characteristics, which would make them be considered ‘infectious’.
What do we mean with ‘prion-like’ characteristics?
We have to first understand that prions are types of proteins which can infect other proteins or cells. Prion disease is very rare and mostly occur when prions enter our body from the outside, for example by ingesting prion-infected food. For Alzheimer’s disease, however, the prions are not coming from outside of the body but it the actual amyloid and tau proteins which behave in the brain ‘like prions’ infecting nerve cell after nerve cell. Therefore amyloid and tau are not considered to be prions themselves but are said to have ‘prion-like’ characteristics.
Does this mean that if we somehow get ‘infected’ with these amyloid and tau proteins that we will develop Alzheimer’s disease?
This has been an ongoing question, which the two recent publications * try to address. Both publications convened panels of experts to review independently the evidence whether there is a danger of getting infected like this.
Both publications reviewed all existing reports which documented cases where there was potential ‘infection’ by amyloid or tau from blood or brain tissue from someone with Alzheimer’s disease. More importantly, they checked that even if such an amyloid or tau ‘infection’ occurred, whether it resulted in the development of Alzheimer’s disease.
The results of both independent studies show clearly that the danger of being ‘infected’ by amyloid or tau is very low if not negligible. This was even the case for high-risk professions, such as neuropathologists and neurosurgeons who work all day directly with brain tissue, and are therefore at the potentially highest risk of being ‘infected’ with amyloid and tau.
Finally, both publications showed that even in the extremely rare cases when someone got ‘infected’ with amyloid or tau by someone who had Alzheimer’s disease, the person infected did not develop Alzheimer’s disease themselves. They could develop other clinical symptoms which can be treated but no one developed Alzheimer’s disease.
There is no reason therefore to be worried about being ‘infected’ by Alzheimer’s disease, even in the rare instance that we require a blood transfusion or have to undergo brain surgery. Finally some good news!
Lauwers E, Lalli G, Brandner S, Collinge J, Compernolle V, Duyckaerts C, Edgren G, Haïk S, Hardy J, Helmy A, Ivinson AJ, Jaunmuktane Z, Jucker M, Knight R, Lemmens R, Lin IC, Love S, Mead S, Perry VH, Pickett J, Poppy G, Radford SE, Rousseau F, Routledge C, Schiavo G, Schymkowitz J, Selkoe DJ, Smith C, Thal DR, Theys T, Tiberghien P, van den Burg P, Vandekerckhove P, Walton C, Zaaijer HL, Zetterberg H, De Strooper B. Potential human transmission of amyloid β pathology: surveillance and risks. Lancet Neurol. 2020 Oct;19(10):872-878. Epub 2020 Sep 16
David M Asher, MD, Ermias Belay, MD, Eileen Bigio, MD, Sebastian Brandner, MD, Scott A Brubaker, BA, Byron Caughey, PhD, Brychan Clark, MD, Inger Damon, MD, PhD, Marc Diamond, MD, Michelle Freund, PhD, Bradley T Hyman, MD, PhD, Mathias Jucker, PhD, C Dirk Keene, MD, PhD, Andrew P Lieberman, MD, PhD, Miroslaw Mackiewicz, PhD, Thomas J Montine, MD, PhD, Susan Morgello, MD, Creighton Phelps, PhD, Jiri Safar, MD, PhD, Julie A Schneider, MD, MS, Lawrence B Schonberger, MD, MPH, Christina Sigurdson, DVM, PhD, Nina Silverberg, PhD, John Q Trojanowski, MD, PhD, Matthew P Frosch, MD, PhD, Risk of Transmissibility From Neurodegenerative Disease-Associated Proteins: Experimental Knowns and Unknowns, Journal of Neuropathology & Experimental Neurology, , nlaa109, https://doi.org/10.1093/jnen/nlaa109
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