No evidence that Alzheimer’s disease might be contagious

Bonn, 14 December, 2018 - Can Alzheimer’s disease be transmitted between individuals? According to British researchers, medical interventions involving the transmission of brain material could pose a potential risk. However, the study does not suggest that Alzheimer’s disease could be contagious in everyday contact with patients with the disease.

“There is no evidence that Alzheimer’s could be contagious. Even the now published results do not change this assessment. Dealing with and caring for Alzheimer’s patients poses no risk,” stresses Prof. Christian Haass, Speaker of the DZNE’s Munich site. “The current study is based on laboratory experiments on mice. It is questionable whether this situation applies to medical interventions on humans as happening today. In the current study, the effects of a hormone obtained from the brains of deceased people were investigated. However, such hormones for the treatment of growth disorders are no longer in use today. They have been produced biotechnologically since 1985. Furthermore, I doubt that brain surgery poses a significant risk.”

The current study follows on from earlier investigations by the same research team that where published in 2015 (Zane Jaunmuktane et al., Nature 2015, DOI: 10.1038/nature15369). At that time, the researchers examined the brains of individuals who had died due to Creutzfeldt-Jakob Disease (CJD). In their childhood, these subjects had been treated with hormones for growth disorders. Until 1985, such growth hormones were derived from the brains of deceased persons. It turned out that the brains of CJD patients exhibited deposits of beta-amyloid proteins in addition to features of CJD. Such deposits (the notorious “plaques”) are among the hallmarks of Alzheimer’s disease. At the time, this finding led to the assumption that the hormone compound might have contained proteins typical of Alzheimer’s that were transferred to the recipients of the hormone treatment. However, the 2015 study did not analyze the hormone compound.

For the current study, the researchers examined old stocks of the compound. In some batches they were actually able to detect proteins typical of Alzheimer’s. In further experiments, the compound was administered to mice by injection. The brains of the mice later developed the amyloid deposits typical of Alzheimer’s. However, this not a new finding: It was already known before that brain extracts from individuals with Alzheimer’s can trigger the formation of plaques in mice. The question as to whether neurosurgical interventions might pose a risk has also been discussed for some time. However, clinical studies have not provided any evidence that Alzheimer’s can actually be transmitted in this way.

Due to the publication in 2015, the hypothesis arose that Alzheimer’s might be a potentially infectious disease. However, there are strong arguments against it, which remain valid:

1) In the original studies on CJD patients, it was only found that these patients had beta-amyloid deposits in the blood vessels of the brain (so-called cerebral amyloid angiopathy), but not that they would actually develop Alzheimer’s. In this context, it is important to note that many people have beta-amyloid deposits in their brains without developing symptoms of Alzheimer’s.

2) In addition, an important part of Alzheimer’s pathology was missing in the original studies on CJD patients. There were amyloid deposits, but no deposits of tau protein. Only the presence of both types of pathology is evidence of Alzheimer’s. Notably, the current study shows that tau is present in the hormone compound.

3) There is no evidence from epidemiological studies that Alzheimer’s could be transmitted through infection.

4) Even animal experiments do not indicate an infection mechanism: For example, healthy mice can be kept in the same cage with mouse models of Alzheimer’s and the healthy mice do not develop Alzheimer’s.

5) For the current study, compounds derived from human brain were injected into the brains of mice. This is a highly artificial situation. There is no comparable situation in clinical practice.

Source: pixabay / geralt

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Original publication

Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone.

Silvia A. Purro et al. Nature. 13. Dezember 2018
DOI: 10.1038/s41586-018-0790-y


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