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Tytuł pozycji:

[A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy].

Tytuł:
[A Therapeutic Target for Inhibition of Neurodegeneration: Autophagy].
Autorzy:
Pupyshev AB
Korolenko TA
Tikhonova MA
Źródło:
Zhurnal vysshei nervnoi deiatelnosti imeni I P Pavlova [Zh Vyssh Nerv Deiat Im I P Pavlova] 2016 Sep; Vol. 66 (5), pp. 515-540.
Typ publikacji:
Journal Article; Review
Język:
Russian
Imprint Name(s):
Publication: Moscow : Izd-Vo Akademiia Nauk Ssr
Original Publication: Moscow, Izd-vo Akademiia nauk SSR.
MeSH Terms:
Alzheimer Disease/*drug therapy
Autophagy/*drug effects
Huntington Disease/*drug therapy
Molecular Targeted Therapy/*methods
Neuroprotective Agents/*therapeutic use
Parkinson Disease/*drug therapy
Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Autophagy/genetics ; Clinical Trials as Topic ; Gene Expression Regulation ; Humans ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Metformin/therapeutic use ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Proteasome Endopeptidase Complex/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Sirolimus/therapeutic use ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Ubiquitin/genetics ; Ubiquitin/metabolism ; alpha-Synuclein/genetics ; alpha-Synuclein/metabolism
Substance Nomenclature:
0 (Amyloid beta-Peptides)
0 (HTT protein, human)
0 (Huntingtin Protein)
0 (Molecular Chaperones)
0 (Neuroprotective Agents)
0 (Ubiquitin)
0 (alpha-Synuclein)
9100L32L2N (Metformin)
EC 2.7.1.1 (MTOR protein, human)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
EC 3.4.25.1 (Proteasome Endopeptidase Complex)
W36ZG6FT64 (Sirolimus)
Entry Date(s):
Date Created: 20190130 Date Completed: 20190219 Latest Revision: 20211204
Update Code:
20240104
PMID:
30695399
Czasopismo naukowe
The role of autophagy in cell survival and suppression of neurodegeneration was considered. We discussed its involvement in Alzheimer's, Parkinson's, and Huntington's diseases connected with accumulation of amy- loid-β, α-synuclein, and huntingtin, respectively. Autophagy is reduced in these diseases and in aging as well to various extent. Elimination of accumulated toxic proteins and structures is performed by autophagy mech- anisms (chaperon-mediated autophagy, macroautophagy, selected autophagy) in an interaction with ubiqui- tin-proteasome system. In many cases activation of mTOR-dependent autophagy and mTOR-independent regulatory pathways lead to the therapeutic effect of inhibition of neurodegeneration in cell cultures and an- imal models. Some autophagy enhancers such as resveratrol, metformin, rilmenidine, lithium, and curcumin are tested now in clinical trials.

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