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. 2020 May 29;15:30. doi: 10.1186/s13024-020-00376-6

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© The Author(s) 2020

Open AccessThis 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/. 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 in a credit line to the data.

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Fig. 2 — Abnormal mitochondrial fusion and fission in AD. (Top) A family of large GTPases regulate balanced mitochondrial fusion (e.g. Mfn1/2, OPA1) and fission (DLP1). For mitochondrial fission, mitochondrial outer membrane proteins (e.g. Fis1, Mff and others) recruit cytosolic DLP1 protein to mitochondria that oligomerize and form a ring structure around fission site. (Bottom) Amyloid-β and other AD related insults cause neuronal calcium influx and increased ROS production that activate downstream proteases (calpain) and protein kinase that act on mitochondrial fission/fusion GTPases and disturb mitochondrial fusion and fission in AD