A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy

A. B. Pupyshev, T. A. Korolenko, M. A. Tikhonova

    Результат исследования: Научные публикации в периодических изданияхстатья

    1 Цитирования (Scopus)

    Аннотация

    The role of autophagy in supporting cellular survival and inhibiting neurodegeneration in Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, which are accompanied by the accumulation of the proteins β-amyloid, α-synuclein, and huntingtin, is discussed. Autophagy undergoes various degrees of weakening in these diseases, and also decreases in aging. Removal of accumulated toxic proteins and structures is mediated by the mechanisms of autophagy (chaperone-mediated autophagy, macroautophagy, mitophagy) in interactions with the ubiquitin-proteasome system. In many cases, activation of mTOR-dependent autophagy and mTOR-independent pathways for its regulation leads to the therapeutic effect of inhibiting neurodegeneration in cell cultures and animal models of diseases. A number of autophagy activators (resveratrol, metformin, rilmenidine, lithium, cucurmin, etc.) are in the stage of clinical trials.

    Язык оригиналаанглийский
    Страницы (с-по)1109-1127
    Число страниц19
    ЖурналNeuroscience and Behavioral Physiology
    Том47
    Номер выпуска9
    DOI
    СостояниеОпубликовано - 1 ноя 2017

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