Autophagy in neurodegeneration: two sides of the same coin

被引:61
作者
Lee, Jin-A [1 ]
机构
[1] Hannam Univ, Coll Life Sci & Nano Technol, Dept Biotechnol, Taejon 305811, South Korea
关键词
Autophagy; Cell death; Cell survival; Neurodegeneration; ALZHEIMER-DISEASE; NERVOUS-SYSTEM; AXONAL DEGENERATION; TRANSGENIC MICE; SELF-DIGESTION; MOUSE MODELS; C-ELEGANS; INHIBITION; ACCUMULATION; TOXICITY;
D O I
10.5483/BMBRep.2009.42.6.324
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy is a bulk lysosomal degradation process important in development differentiation and cellular homeostasis in multiple organs. Interestingly, neuronal survival is highly dependent on autophagy due to its post-mitotic nature, polarized morphology and active protein trafficking. A growing body of evidence now suggests that alteration or dysfunction of autophagy causes accumulation of abnormal proteins and/or damaged organelles, thereby leading to neurodegenerative disease. Although autophagy generally prevents neuronal cell death, it plays a protective or detrimental role in neurodegenerative disease depending on the environment In this review, the two sides of autophagy will be discussed in the context of several neurodegenerative diseases. [BMB reports 2009; 42(6): 324-330]
引用
收藏
页码:324 / 330
页数:7
相关论文
共 48 条
[1]   Autophagy is disrupted in a knock-in mouse model of juvenile neuronal ceroid lipofuscinosis [J].
Cao, Yi ;
Espinola, Janice A. ;
Fossale, Elisa ;
Massey, Ashish C. ;
Cuervo, Ana Maria ;
MacDonald, Marcy E. ;
Cotman, Susan L. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (29) :20483-20493
[2]   Protofibrils, pores, fibrils, and neurodegeneration: Separating the responsible protein aggregates from the innocent bystanders [J].
Caughey, B ;
Lansbury, PT .
ANNUAL REVIEW OF NEUROSCIENCE, 2003, 26 :267-298
[3]   New insights into the mechanisms of macroautophagy in mammalian cells [J].
Eskelinen, Eeva-Liisa .
INTERNATIONAL REVIEW OF CELL AND MOLECULAR BIOLOGY, VOL 266, 2008, 266 :207-247
[4]   Neuronal loss and brain atrophy in mice lacking cathepsins B and L [J].
Felbor, U ;
Kessler, B ;
Mothes, W ;
Goebel, HH ;
Ploegh, HL ;
Bronson, RT ;
Olsen, BR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (12) :7883-7888
[5]   Functional multivesicular bodies are required for autophagic clearance of protein aggregates associated with neurodegenerative disease [J].
Filimonenko, Maria ;
Stuffers, Susanne ;
Raiborg, Camilla ;
Yamamoto, Ai ;
Malerod, Lene ;
Fisher, Elizabeth M. C. ;
Isaacs, Adrian ;
Brech, Andreas ;
Stenmark, Harald ;
Simonsen, Anne .
JOURNAL OF CELL BIOLOGY, 2007, 179 (03) :485-500
[6]   Ambra1 regulates autophagy and development of the nervous system [J].
Fimia, Gian Maria ;
Stoykova, Anastassia ;
Romagnoli, Alessandra ;
Giunta, Luigi ;
Di Bartolomeo, Sabrina ;
Nardacci, Roberta ;
Corazzari, Marco ;
Fuoco, Claudia ;
Ucar, Ahmet ;
Schwartz, Peter ;
Gruss, Peter ;
Piacentini, Mauro ;
Chowdhury, Kamal ;
Cecconi, Francesco .
NATURE, 2007, 447 (7148) :1121-U14
[7]   Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice [J].
Hara, Taichi ;
Nakamura, Kenji ;
Matsui, Makoto ;
Yamamoto, Akitsugu ;
Nakahara, Yohko ;
Suzuki-Migishima, Rika ;
Yokoyama, Minesuke ;
Mishima, Kenji ;
Saito, Ichiro ;
Okano, Hideyuki ;
Mizushima, Noboru .
NATURE, 2006, 441 (7095) :885-889
[8]   All-you-can-eat: autophagy in neurodegeneration and neuroprotection [J].
Jaeger, Philipp A. ;
Wyss-Coray, Tony .
MOLECULAR NEURODEGENERATION, 2009, 4
[9]   Aberrant molecular properties shared by familial Parkinson's disease-associated mutant UCH-L1 and carbonyl-modified UCH-L1 [J].
Kabuta, Tomohiro ;
Setsuie, Rieko ;
Mitsui, Takeshi ;
Kinugawa, Aiko ;
Sakurai, Mikako ;
Aoki, Shunsuke ;
Uchida, Kenko ;
Wada, Keiji .
HUMAN MOLECULAR GENETICS, 2008, 17 (10) :1482-1496
[10]   Huntingtin expression stimulates endosomal-lysosomal activity, endosome tubulation, and autophagy [J].
Kegel, KB ;
Kim, M ;
Sapp, E ;
McIntyre, C ;
Castaño, JG ;
Aronin, N ;
DiFiglia, M .
JOURNAL OF NEUROSCIENCE, 2000, 20 (19) :7268-7278