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Journal of NeurochemistryVolume 168, Issue 2 p. 67-68 ISSUE INFORMATIONFree Access Issue Information First published: 24 January 2024 https://doi.org/10.1111/jnc.15854 Read the full article: ‘Over-expression of N-acetylaspartate synthase exacerbates pathological energetic deficit and accelerates cognitive decline in the 5xFAD mouse’ by J. S. Francis, Q. Nguyen, V. Markov and P. Leone (J. Neurochem. vol. 168 (2), pp. 69–82) on doi: 10.1111/jnc.16044 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Graphical Abstract Front cover Increasing NAA synthase (Nat8L) via AAV-mediated overexpression in a model of Alzheimer's Disease compromises mitochondrial energy metabolism. Sequestration of mitochondrial aspartate by NAA is incompatible with pathological energetic crisis, accelerates associated cognitive decline and presents a rationale for the active reduction of NAA in a broad clinical spectrum of neurodegenerative disease. Image content Overexpression of NAA synthase (Nat8L) in hippocampal Neurons of 5xFAD mice compounds phenotypic energy deficit and accelerates cognitive decline. Read the full article ‘Over-expression of N-acetylaspartate synthase exacerbates pathological energetic deficit and accelerates cognitive decline in the 5xFAD mouse’ by J. S. Francis, Q. Nguyen, V. Markov and P. Leone (J. Neurochem. vol. 168 (2), pp. 69–82) on doi: 10.1111/jnc.16044 Volume168, Issue2February 2024Pages 67-68 RelatedInformation