期刊
NEUROSCIENCE LETTERS
卷 697, 期 -, 页码 34-48出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2018.04.006
关键词
ALS; Alsin; Autophagy; C9orf72; CHMP2B; Dynactin; FIG4; FTD; FUS; Optineurin; p62; Profilin; SOD1; TBK1; TDP-43; VAPB; VCP; UBQLN2
资金
- NIH [NS074324, NS089616]
- Robert Packard Center for ALS Research at Johns Hopkins
- ALS Association
- Muscular Dystrophy Association
- Department of Defense
- Judith & Jean Page Adams Chritable Foundation
Age-dependent neurodegenerative diseases are associated with a decline in protein quality control systems including autophagy. Amyotrophic lateral sclerosis (ALS) is a motor neuron degenerative disease of complex etiology with increasing connections to other neurodegenerative conditions such as frontotemporal dementia. Among the diverse genetic causes for ALS, a striking feature is the common connection to autophagy and its associated pathways. There is a recurring theme of protein misfolding as in other neurodegenerative diseases, but importantly there is a distinct common thread among ALS genes that connects them to the cascade of autophagy. However, the roles of autophagy in ALS remain enigmatic and it is still unclear whether activation or inhibition of autophagy would be a reliable avenue to ameliorate the disease. The main evidence that links autophagy to different genetic forms of ALS is discussed.
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