MFN2 and Alzheimer disease: In summary, our study not only details behavioral impairments together with deposition of amyloid plaque and neuroinflammation and disrupted mitochondrial bioenergetics in an age-dependent manner, which strongly support the suitability of APPKI mice in the research of AD, but our result also suggests mitochondrial dysfunction as a very early event in the AD pathogenesis and proposed a potential therapeutic target, MFN2, for the treatment of AD.