Age-related amyloidosis outside the brain: A state-of-the-art review
Age-related amyloidosis outside the brain: A state-of-the-art review
复制标题
大脑外与年龄相关的淀粉样变性:最新综述
DOI:
10.1016/j.arr.2021.101388
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发表时间:
2021
期刊:
影响因子:
13.1
通讯作者:
Ueda M.
中科院分区:
文献类型:
--
作者:
Tasaki M;Lavatelli F;Obici L;Obayashi K;Miyamoto T;Merlini G;Palladini G;Ando Y;Ueda M.
Inside and outside the brain, accumulation of amyloid fibrils plays key roles in the pathogenesis of fatal age-related diseases such as Alzheimer’s and Parkinson’s diseases and wild-type transthyretin amyloidosis. Although the incidence of all amyloidoses increases with age, for some types of amyloidosis aging is known as the main direct risk factor, and these types are typically diseases of elderly people. More than 10 different precursor proteins are known to cause age-associated amyloidosis; these proteins include amyloid β protein, α-synuclein, transthyretin, islet amyloid polypeptide, atrial natriuretic factor, and the newly discovered epidermal growth factor-containing fibulin-like extracellular matrix protein 1. Except for intracerebral amyloidoses, most age-related amyloidoses have been little studied. Indeed, in view of the increasing life expectancy in our societies, understanding how aging is involved in the process of amyloid fibril accumulation and the effects of amyloid deposits on the aging body is extremely important. In this review, we summarize current knowledge about the nature of amyloid precursor proteins, the prevalence, clinical manifestations, and pathogenesis of amyloidosis, and recent advances in our understanding of age-related amyloidoses outside the brain.