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. 2016 Jul 11;11:50. doi: 10.1186/s13024-016-0119-y

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© The Author(s). 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 1 — Multifactorial nature of AD and involvement of several different etiopathogenic mechanisms. Early-onset familial AD caused by mutations in APP, PS1, or PS2 constitutes < 1 % of AD cases. The exact causes of late-onset sporadic AD which accounts for the remaining > 99 % of AD cases are as yet largely unknown. However, aging alongside gene-environment interaction is speculated to contribute to this form of AD. Both forms of AD lead to amyloid plaque and neurofibrillary pathologies, synaptic dysfunction and neurodegeneration, and ultimately cognitive impairment