Facts and speculations on the infectious nature of Alzheimer’s disease

Abstract

For over 30 years, a large volume of data has been collected indicating the possibility of an infectious form of Alzheimer’s disease (AD). Using various AD animal models and patients’ brain extracts it has been demonstrated that amyloid Aβ (Aβ) can be an infectious agent. The similarities of Aβ and PrPsc prion protein (PrPsc) have been an important indicator of a potentially infective nature of AD. Nonetheless, the majority of epidemiological data have not yet supported the hypothesis of the infectious nature of this disease. It must be emphasized that AD is a very complex disease which is most likely unique to humans. The strong evidence on the infectivity and propagation of Aβ in animal models is accompanied by the uncertainty of whether the observed symptoms can be recapitulated in humans. Therefore, using currently available AD models it may not be feasible to collect data of sufficient quality clearly and unambiguously demonstrating the infectivity of the disease. We postulate that in order to gather stronger evidence for AD infectivity in humans, new experimental strategies must be considered. This approach should also lead to better understanding of the peripheral routes of Aβ infection. The aim of this review is to present the current state of knowledge and existing doubts in this important area of neurobiology and medicine. In the light of available data, AD infectivity has still not been proven, yet it should be seriously considered. The confirmation that some forms of AD are infectious may result in significant scientific, medical and social consequences.