A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy

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

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    1 Citation (Scopus)


    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.

    Original languageEnglish
    Pages (from-to)1109-1127
    Number of pages19
    JournalNeuroscience and Behavioral Physiology
    Issue number9
    Publication statusPublished - 1 Nov 2017


    • Alzheimer’s disease
    • autophagy
    • autophagy inducers
    • huntingtin
    • Huntington’s disease
    • neurodegeneration
    • Parkinson’s disease
    • proteasomes
    • α-synuclein
    • β-amyloid

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