By Helen Luojia Zhang
Alzheimer’s disease is a chronic neurodegenerative disease which acts as the most common cause of dementia. Alzheimer’s is typically characterized by cognitive impairment such as loss of memory, confusion and mood changes. As the disease progresses, patients suffer from more severe symptoms, including aphasia and dysphagia. In the brain of people with this neurological condition, abnormally folded amyloid-beta protein clumps into whitish plaques and hyperphosphorylated tau protein twists into tangles (Ising, Stanley and Holtzman, 2015). This disrupts the connection between nerve cells, ultimately leading to cell death.
Back in the 1950s, thousands of children with growth disorder were injected with growth hormone derived from pituitary glands of human cadavers. This treatment was forced to cease in 1985 when a few patients who received the injection had developed Creutzfeldt-Jakob disease (CJD), another degenerative brain disorder, due to the prion-contaminated growth hormone (Jaunmuktane et al., 2015). Misfolded prion proteins have infectious nature that can transfer its misfolded shape to normal cellular prion proteins nearby, inducing an amplification cascade of transmissible prions in a process known as ‘seeding’ (Derkinderen, 2019). Unexpectedly, in addition to abnormal prion proteins, in the autopsy of brain tissues of eight individuals with CJD, amyloid-beta protein deposition, a typical hallmark of Alzheimer’s Disease, was found in the grey matter of four patients. This suggests transmission of Alzheimer’s from an affected individual may be possible (Jaunmuktane et al., 2015).
Later on, experiments on animal models have further proved the seeding activities of amyloid-beta proteins. In this experiment, diluted amyloid-beta containing brain extracts from humans with Alzheimer’s were injected into the brain of transgenic mice, which had induced numerous amyloid-beta deposits in the brain of mice after four months (Meyer-Luehmann et al., 2006). This suggests amyloid-beta protein may have a prion-like transmission mechanism.
Prion diseases like CJD can be transmitted through common medical procedures such as blood transfusion or organ transplant (Bu, Li and Wang, 2019). Therefore, there is a rising concern that amyloid-beta protein involved in Alzheimer’s is also transmissible due to its prion-like behaviour. Ever since then, whether Alzheimer’s is transmissible between humans has become a highly concerning public health issue.
However, a cohort study between 1968 and 2012, where data of 1,465,845 patients who received blood transfusion were collected, showed that there is no increased risk to catch Alzheimer’s due to blood transfusion (Edgren et al., 2016). The hazard ratio for patients receiving blood transfusion from donors who develop Alzheimer’s symptoms later in their lives versus those receiving blood from healthy donors was 1.04, indicating no evidence of transfusion transmission of Alzheimer’s Disease (Edgren et al., 2016).
It has also been reported parenchymal amyloid-beta plaques are more likely to be found in CJD cases after dura mater grafts than sporadic CJD, indicating the possibility that amyloid-beta proteins could be spread through contaminated surgical equipment (Frontzek et al., 2016). So far, however, there is no valid evidence showing Alzheimer’s disease is capable of transmitting through medical equipment since alternative explanations for the results may also be possible.
In conclusion, Alzheimer’s is not a contagious disease, meaning it does not spread through physical contact. That said, even though there is currently no conclusive evidence of amyloid-beta pathology transmission directly between humans, the potential transmission risk should not be ignored. It is essential to carry out preventative measures in clinics and keep track of those patients in the past experiments due to the long incubation period of Alzheimer’s Disease.
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Derkinderen, P. (2019) ‘Could it be that neurodegenerative diseases are infectious?’, Revue Neurologique, 175(7–8), pp. 427–430. doi: 10.1016/j.neurol.2019.07.003.
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Frontzek, K et al., (2016). Amyloid-β pathology and cerebral amyloid angiopathy are frequent in iatrogenic Creutzfeldt-Jakob disease after dural grafting. Swiss medical weekly, 146, p.w14287.
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Jaunmuktane, Z. et al. (2015) ‘Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy’, Nature, 525(7568), pp. 247–250. doi: 10.1038/nature15369.
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