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. 2021 Aug 31;6:325. doi: 10.1038/s41392-021-00748-4

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — A proposed role of the ACAA1 p.N299S-mediated lysosomal dysfunction and impaired autophagy in the development of AD. ACAA1 p.N299S has an impaired enzymatic activity, affects autophagy and lysosomal function, subsequently contributes to the aggravation of the Aβ pathology and neuronal loss, and finally causes cognitive impairment and other AD-related symptoms