Biochemical Society transactions · 2024
Exploring potential developmental origins of common neurodegenerative disorders.
СтатьяОбзорПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Catlin James P, Schaner Tooley Christine E
Аннотация
In the United States, it is now estimated that 6.7 million people over the age of 65 are afflicted by Alzheimer's disease (AD), over 1 million people are living with Parkinson's disease (PD), and over 200 000 have or are at risk for developing Huntington's disease (HD). All three of these neurodegenerative diseases result in the ultimate death of distinct neuronal subtypes, and it is widely thought that age-related damage is the single biggest contributing factor to this neuronal death. However, recent studies are now suggesting that developmental defects during early neurogenesis could also play a role in the pathology of neurodegenerative diseases. Loss or overexpression of proteins associated with HD, PD, and AD also result in embryonic phenotypes but whether these developmental defects slowly unmask over time and contribute to age-related neurodegeneration remains highly debated. Here, we discuss known links between embryonic neurogenesis and neurodegenerative disorders (including common signaling pathways), potential compensatory mechanisms that could delay presentation of neurodegenerative disorders, and the types of model systems that could be used to study these links in vivo.