TY - CHAP

T1 - Autophagy and neurodegeneration

AU - Korolenko, T. A.

AU - Pupyshev, A. B.

AU - Pospelova, T. I.

AU - Gritsyk, O. B.

AU - Panov, A. V.

AU - Vavilin, V. A.

AU - Shintyapina, A. B.

AU - Tikhonova, M. A.

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Neurodegenerative diseases are widespread disorders, with prevalence increasing with age. Effectiveness of their treatment depends on understanding of their etiology, which is not clear at present. In this regard, the key mechanisms of their development and various new approaches to treatment are important. A common feature of these diseases is the accumulation of proteins prone to aggregation and protein inclusions, which are markers of these diseases and have pathogenetic significance. The cellular tool for their elimination is autophagy. The latter is an intracellular phenomenon: the transfer of own cytoplasmic material into autophagosomes, followed by fusion with lysosomes, leading to enzymatic degradation of the material in question and reuse of monomers in biosynthetic processes. The roles of autophagy in maintaining cellular survival and in suppression of neurodegeneration have been evaluated in Alzheimer’s, Parkinson’s, and Huntington’s diseases, which are accompanied by the accumulation of β-amyloid, α- synuclein, and huntingtin, respectively. Autophagy is weakened in various ways in these diseases and decreases with ageing. The removal of the accumulating toxic proteins and structures is carried out by the mechanisms of autophagy (chaperone-mediated autophagy, macroautophagy, and mitophagy) during interaction with the ubiquitin-proteasome system. The pathogenesis and treatment of neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s diseases and amyotrophic lateral sclerosis) require elucidation and the development of new approaches, respectively. Neurodegenerative diseases combine disturbances in certain brain structures (lysosomes and lysosomal proteases), which, in the presence of the characteristics of each disease, include some common molecular and cellular mechanisms.

AB - Neurodegenerative diseases are widespread disorders, with prevalence increasing with age. Effectiveness of their treatment depends on understanding of their etiology, which is not clear at present. In this regard, the key mechanisms of their development and various new approaches to treatment are important. A common feature of these diseases is the accumulation of proteins prone to aggregation and protein inclusions, which are markers of these diseases and have pathogenetic significance. The cellular tool for their elimination is autophagy. The latter is an intracellular phenomenon: the transfer of own cytoplasmic material into autophagosomes, followed by fusion with lysosomes, leading to enzymatic degradation of the material in question and reuse of monomers in biosynthetic processes. The roles of autophagy in maintaining cellular survival and in suppression of neurodegeneration have been evaluated in Alzheimer’s, Parkinson’s, and Huntington’s diseases, which are accompanied by the accumulation of β-amyloid, α- synuclein, and huntingtin, respectively. Autophagy is weakened in various ways in these diseases and decreases with ageing. The removal of the accumulating toxic proteins and structures is carried out by the mechanisms of autophagy (chaperone-mediated autophagy, macroautophagy, and mitophagy) during interaction with the ubiquitin-proteasome system. The pathogenesis and treatment of neurodegenerative diseases (Alzheimer’s, Parkinson’s, Huntington’s diseases and amyotrophic lateral sclerosis) require elucidation and the development of new approaches, respectively. Neurodegenerative diseases combine disturbances in certain brain structures (lysosomes and lysosomal proteases), which, in the presence of the characteristics of each disease, include some common molecular and cellular mechanisms.

KW - Autophagy

KW - Cysteine proteases

KW - Lysosomes

KW - Neurodegeneration

UR - http://www.scopus.com/inward/record.url?scp=85034739765&partnerID=8YFLogxK

M3 - Chapter

AN - SCOPUS:85034739765

SN - 9781536122473

SP - 1

EP - 34

BT - Neurodegenerative Diseases

PB - Nova Science Publishers, Inc.

ER -