The amyloid cascade hypothesis of Alzheimer’s Disease (Hardy & Higgins, 1992[1]) suggests that in Alzheimer’s Disease, sticky amyloid-beta (Aß) peptides fail to be removed from extracellular space in the brain. These peptides become amyloid plaques. Similarly, intracellular tau proteins fold irregularly into neurofibrillary tangles which destroy cells. Although not without its critics (e.g., Drachman, 2014[2]), the model has received much support. Lista et al. (2014)[3], for example, described it as the best accepted model for explaining the pathogenesis of AD.
[1] Hardy, J. A., & Higgins, G. A. (1992). Alzheimer’s Disease: The Amyloid Cascade Hypothesis. Science, 256(5054), 184–185. http://www.jstor.org/stable/2876981
[2] Drachman, D. A. (2014). The amyloid hypothesis, time to move on: Amyloid is the downstream result, not cause, of Alzheimer’s disease. Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, 10(3), 372–380. https://doi.org/10.1016/j.jalz.2013.11.003
[3] Lista, S., Garaci, F. G., Ewers, M., Teipel, S., Zetterberg, H., Blennow, K., & Hampel, H. (2014). CSF Aβ1-42 combined with neuroimaging biomarkers in the early detection, diagnosis and prediction of Alzheimer’s disease. Alzheimer’s & Dementia, 10(3), 381–392. https://doi.org/10.1016/j.jalz.2013.04.506
