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A Therapeutic Target for Inhibition of Neurodegeneration : Autophagy. / Pupyshev, A. B.; Korolenko, T. A.; Tikhonova, M. A.

In: Neuroscience and Behavioral Physiology, Vol. 47, No. 9, 01.11.2017, p. 1109-1127.

Research output: Contribution to journal › Article › peer-review

Harvard

Pupyshev, AB, Korolenko, TA & Tikhonova, MA 2017, 'A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy', Neuroscience and Behavioral Physiology, vol. 47, no. 9, pp. 1109-1127. https://doi.org/10.1007/s11055-017-0519-7

APA

Pupyshev, A. B., Korolenko, T. A., & Tikhonova, M. A. (2017). A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy. Neuroscience and Behavioral Physiology, 47(9), 1109-1127. https://doi.org/10.1007/s11055-017-0519-7

Vancouver

Pupyshev AB, Korolenko TA, Tikhonova MA. A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy. Neuroscience and Behavioral Physiology. 2017 Nov 1;47(9):1109-1127. doi: 10.1007/s11055-017-0519-7

Author

Pupyshev, A. B. ; Korolenko, T. A. ; Tikhonova, M. A. / A Therapeutic Target for Inhibition of Neurodegeneration : Autophagy. In: Neuroscience and Behavioral Physiology. 2017 ; Vol. 47, No. 9. pp. 1109-1127.

BibTeX

@article{fa7c5887cc084a7d85ba38d8ef7af553,
title = "A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy",
abstract = "The role of autophagy in supporting cellular survival and inhibiting neurodegeneration in Alzheimer{\textquoteright}s disease, Parkinson{\textquoteright}s disease, and Huntington{\textquoteright}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.",
keywords = "Alzheimer{\textquoteright}s disease, autophagy, autophagy inducers, huntingtin, Huntington{\textquoteright}s disease, neurodegeneration, Parkinson{\textquoteright}s disease, proteasomes, α-synuclein, β-amyloid",
author = "Pupyshev, {A. B.} and Korolenko, {T. A.} and Tikhonova, {M. A.}",
year = "2017",
month = nov,
day = "1",
doi = "10.1007/s11055-017-0519-7",
language = "English",
volume = "47",
pages = "1109--1127",
journal = "Neuroscience and Behavioral Physiology",
issn = "0097-0549",
publisher = "Springer New York",
number = "9",

}

RIS

TY - JOUR

T1 - A Therapeutic Target for Inhibition of Neurodegeneration

T2 - Autophagy

AU - Pupyshev, A. B.

AU - Korolenko, T. A.

AU - Tikhonova, M. A.

PY - 2017/11/1

Y1 - 2017/11/1

N2 - 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.

AB - 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.

KW - Alzheimer’s disease

KW - autophagy

KW - autophagy inducers

KW - huntingtin

KW - Huntington’s disease

KW - neurodegeneration

KW - Parkinson’s disease

KW - proteasomes

KW - α-synuclein

KW - β-amyloid

UR - http://www.scopus.com/inward/record.url?scp=85034220265&partnerID=8YFLogxK

U2 - 10.1007/s11055-017-0519-7

DO - 10.1007/s11055-017-0519-7

M3 - Article

AN - SCOPUS:85034220265

VL - 47

SP - 1109

EP - 1127

JO - Neuroscience and Behavioral Physiology

JF - Neuroscience and Behavioral Physiology

SN - 0097-0549

IS - 9

ER -

ID: 9674254