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<p>Early-onset Alzheimer’s disease (EOAD) is a form of Alzheimer’s disease (AD) that usually manifests before the age of 65 years and is closely linked with a genetic mutation in the amyloid precursor protein (<i>APP</i>) gene. The processing of <i>APP</i> leads to amyloid-beta (Aβ) peptides, which combine to form plaques, a defining feature of Alzheimer’s disease. Neurodegeneration is accelerated by APP mutations, resulting in altered peptide characteristics or increased pathogenic amyloid-beta 42 (Aβ42) isoform synthesis. In this mini-review, we discuss the molecular pathways by which APP mutations cause EOAD and current treatment approaches that target APP-related circuits. Understanding how APP mutations contribute to EOAD of Alzheimer’s disease will help us in improving medicinal approaches for early intervention and treatment.</p>

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Early-Onset Alzheimer’s disease and amyloid precursor protein gene mutations

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Vanlalrinchhani Varte,
  • Lalengkimi Ralte,
  • Nachimuthu Senthil Kumar

摘要

Early-onset Alzheimer’s disease (EOAD) is a form of Alzheimer’s disease (AD) that usually manifests before the age of 65 years and is closely linked with a genetic mutation in the amyloid precursor protein (APP) gene. The processing of APP leads to amyloid-beta (Aβ) peptides, which combine to form plaques, a defining feature of Alzheimer’s disease. Neurodegeneration is accelerated by APP mutations, resulting in altered peptide characteristics or increased pathogenic amyloid-beta 42 (Aβ42) isoform synthesis. In this mini-review, we discuss the molecular pathways by which APP mutations cause EOAD and current treatment approaches that target APP-related circuits. Understanding how APP mutations contribute to EOAD of Alzheimer’s disease will help us in improving medicinal approaches for early intervention and treatment.