Lycium ruthenicum Murr. treatment attenuates APPSWE/PS1ΔE9 mouse model-like mitochondrial dysfunction in Slc25a46 knockout mouse modelMin

Mitochondrial dysfunction is proposed to be substantially associated with ageing and ageing-related diseases like Alzheimer's disease (AD). However, it is unclear whether different mouse models with mitochondrial-related diseases have similar changes in mitochondrial morphology of the same tissues. Moreover, whether similarities in mitochondrial morphology can be a suitable marker for screening and/or discovering mitochondrial-protective substances remains unknown. Mitochondria morphology in different tissues of a novel mitochondrial outer membrane protein Slc25a46 knockout mouse and a traditional APP(SWE)/PS1 Delta E9 transgenic mouse were examined using transmission electron microscope (TEM). Both young Slc25a46 knockout mice and aged APP(SWE)/PS1 Delta E9 mice models showed similar mitochondrial damage in cerebellum tissues. The results indicated that different mitochondrial-related diseases shared similar alteration and defects in mitochondrial morphology. Furthermore, Lycium ruthenicum Murr. extract, a bioactive food substance with cognition-improving property, could effectively improve muscle strength and increase body weight in the Slc25a46 knockout mice. These fndings suggest that mitochondrial morphology defects in mice models, particularly in the mitochondrial compartment, represent a unified and effective marker for screening and validating natural product-derived functional substances with mitochondrial protective properties. It also holds potential application in mitochondrial-impaired senile neurodegenerative diseases, especially in AD. (c) 2023 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Automated summary

Mitochondrial dysfunction is closely associated with aging and aging-related diseases, such as Alzheimer's disease. It is unclear if different mouse models with mitochondrial-related diseases exhibit similar changes in mitochondrial morphology in the same tissues. Additionally, it is unknown if similarities in mitochondrial morphology can be used as a marker for screening and discovering mitochondrial-protective substances.