Bio-Metal Dyshomeostasis-Associated Acceleration of Aging and Cognitive Decline in Down Syndrome

  • Ishihara Keiichi
    Department of Pathological Biochemistry (Currently known as Laboratory of Pathological Biochemistry), Kyoto Pharmaceutical University
  • Kawashita Eri
    Department of Pathological Biochemistry (Currently known as Laboratory of Pathological Biochemistry), Kyoto Pharmaceutical University
  • Akiba Satoshi
    Department of Pathological Biochemistry (Currently known as Laboratory of Pathological Biochemistry), Kyoto Pharmaceutical University

書誌事項

公開日
2023-09-01
資源種別
journal article
DOI
  • 10.1248/bpb.b23-00131
公開者
公益社団法人 日本薬学会

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説明

<p>Down syndrome (DS), which is caused by triplication of human chromosome 21 (Hsa21), exhibits some physical signs of accelerated aging, such as graying hair, wrinkles and menopause at an unusually young age. Development of early-onset Alzheimer’s disease, which is frequently observed in adults with DS, is also suggested to occur due to accelerated aging of the brain. Several Hsa21 genes are suggested to be responsible for the accelerated aging in DS. In this review, we summarize these candidate genes and possible molecular mechanisms, and discuss the related key factors. In particular, we focus on copper, an essential trace element, as a key factor in the accelerated aging in DS. In addition, the physiological significance of brain copper accumulation in cognitive impairment is discussed. We herein provide our hypothesis on the copper dyshomeostasis-based pathophysiology of DS.</p>

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