Article

Amyloid Beta Glycation Induces Neuronal Mitochondrial Dysfunction and Alzheimer’s Pathogenesis via VDAC1-Dependent mtDNA Efflux

2024-05-14

Abstract excerpt

Glycation, the non-enzymatic attachment of reactive dicarbonyls to proteins, lipids, or nucleic acids, contributes to the formation of advanced glycation end-products (AGEs). In Alzheimer’s disease (AD), amyloid-beta (Aβ) undergoes post-translational glycation to produce glycated Aβ (gAβ), yet its pathological role remains poorly understood. Here, we demonstrate that gAβ promotes neuronal mitochondrial DNA (mtDNA)...

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Literature Corpus work: 17ef5eae-ed43-5e5a-ae60-94ee437855cb
DOI: 10.1101/2024.05.14.594173

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Amyloid Beta Glycation Induces Neuronal Mitochondrial Dysfunction and Alzheimer’s Pathogenesis via VDAC1-Dependent mtDNA EffluxDOI 10.1101/2024.05.14.594173Read

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