https://scholars.lib.ntu.edu.tw/handle/123456789/470012
Title: | Autophagy: A double-edged sword in Alzheimer's disease | Authors: | Tung Y.-T. Wang B.-J. Hu M.-K. WEN-MING HSU Lee H. Huang W.-P. Liao Y.-F. |
Issue Date: | 2012 | Journal Volume: | 37 | Journal Issue: | 1 | Start page/Pages: | 157-165 | Source: | Journal of Biosciences | Abstract: | Autophagy is a major protein degradation pathway that is essential for stress-induced and constitutive protein turnover. Accumulated evidence has demonstrated that amyloid-β (Aβ) protein can be generated in autophagic vacuoles, promoting its extracellular deposition in neuritic plaques as the pathological hallmark of Alzheimer's disease (AD). The molecular machinery for Aβ generation, including APP, APP-C99 and β-/γ-secretases, are all enriched in autophagic vacuoles. The induction of autophagy can be vividly observed in the brain at early stages of sporadic AD and in an AD transgenic mouse model. Accumulated evidence has also demonstrated a neuroprotective role of autophagy in mediating the degradation of aggregated proteins that are causative of various neurodegenerative diseases. Autophagy is thus widely regarded as an intracellular hub for the removal of the detrimental Aβ peptides and Tau aggregates. Nonetheless, compelling data also reveal an unfavorable function of autophagy in facilitating the production of intracellular Aβ. The two faces of autophagy on the homeostasis of Aβ place it in a very unique and intriguing position in AD pathogenesis. This article briefly summarizes seminal discoveries that are shedding new light on the critical and unique roles of autophagy in AD and potential therapeutic approaches against autophagy-elicited AD. ? 2011 Indian Academy of Sciences. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84859743802&doi=10.1007%2fs12038-011-9176-0&partnerID=40&md5=29bc4838dd412b31a31964dd18710e23 https://scholars.lib.ntu.edu.tw/handle/123456789/470012 |
ISSN: | 0250-5991 | DOI: | 10.1007/s12038-011-9176-0 | SDG/Keyword: | amyloid beta protein; amyloid precursor protein; beta secretase; galantamine; gamma secretase; ghrelin; lithium; nicotinamide; nilvadipine; tau protein; enzyme activity; homeostasis; modeling; nervous system disorder; protein; rodent; Alzheimer disease; autophagy; disease model; homeostasis; human; nerve degeneration; neuroprotection; nonhuman; pathogenesis; protein aggregation; protein degradation; protein synthesis; review; transgenic mouse; Alzheimer Disease; Amyloid beta-Peptides; Animals; Autophagy; Homeostasis; Humans; Mice; Mice, Transgenic; Proteolysis; tau Proteins; Vacuoles; Mus musculus |
Appears in Collections: | 醫學系 |
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