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Accumulation of amyloid β (Aβ) peptide in the brain is a characteristic pathological feature of Alzheimer’s disease that occurs several decades before the onset of symptoms. Aβ is produced from the membrane-bound amyloid β precursor protein (APP) by β-secretase 1 (BACE1) and γ-secretase-mediated proteolytic cleavage. Alternatively, ADAM10/17 α-secretase and γ-secretase cleavage does not generate Aβ. Accumulating evidence indicates that intracellular trafficking of APP to each secretase determines the level of Aβ production. In this chapter, we summarize how glycosylation affects the Aβ production, possibly by modulating the intracellular localization of APP and its secretases.

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Unique Expression and Glycosylation of Amyloid Precursor Protein in Alzheimer’s Disease

  • 章节

  • 发表日期：

    2026年

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  • Yuriko Tachida,
  • Shinobu Kitazume

摘要

Accumulation of amyloid β (Aβ) peptide in the brain is a characteristic pathological feature of Alzheimer’s disease that occurs several decades before the onset of symptoms. Aβ is produced from the membrane-bound amyloid β precursor protein (APP) by β-secretase 1 (BACE1) and γ-secretase-mediated proteolytic cleavage. Alternatively, ADAM10/17 α-secretase and γ-secretase cleavage does not generate Aβ. Accumulating evidence indicates that intracellular trafficking of APP to each secretase determines the level of Aβ production. In this chapter, we summarize how glycosylation affects the Aβ production, possibly by modulating the intracellular localization of APP and its secretases.