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. 2020 Sep 11;10:14980. doi: 10.1038/s41598-020-72168-3

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Potential impact of increased BACE1 activity in the pathogenesis of VaD, MIXED and LOAD. Cerebrovascular dysfunctions and/or other endogen/exogenous factors (e.g. oxidative stress, genetic predisposition, etc.) may cause increase in BACE1 activity leading to an increase in Aβ formation. This, in turn, can be accompanied by different levels of Aβ clearance efficiency and, as a consequence, by different levels of Aβ brain accumulation. The scenarios that can take place from different combination of increased BACE1/Aβ clearance effectiveness might predispose elderly individuals to different type of dementia: 1) VaD: partially impaired or unaffected Aβ clearance – mild increase/unchanged levels of Aβ 2) MIXED: partially impaired Aβ clearance—moderate to high levels of Aβ 3) LOAD: impaired Aβ clearance- high levels of Aβ.