期刊
TRENDS IN NEUROSCIENCES
卷 39, 期 4, 页码 221-234出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2016.02.002
关键词
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资金
- National Institutes of Health (NIH) [NS093652, AG020670, NS076117, R01]
- Belfer Neurodegeneration Consortium
- Italian Telethon Foundation
- Beyond Batten Disease Foundation
- European Research Council
- NIH [R01 NS 078072-01A1]
The autophagy-lysosomal pathway (ALP) is involved in the degradation of long-lived proteins. Deficits in the ALP result in protein aggregation, the generation of toxic protein species, and accumulation of dysfunctional organelles, which are hallmarks of Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and prion disease. Decades of research have therefore focused on enhancing the ALP in neurodegenerative diseases. More recently, transcription factor EB (TFEB), a major regulator of autophagy and lysosomal biogenesis, has emerged as a leading factor in addressing disease pathology. We review the regulation of the ALP and TFEB and their impact on neurodegenerative diseases. We also offer our perspective on the complex role of autophagy and TFEB in disease pathogenesis and its therapeutic implications through the examination of prion disease.
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