Abstract
Autophagy is a tightly regulated lysosomal degradation/recycling pathway, critical for cellular homeostasis, such as neuronal survival and death. Impaired autophagic function has been reported in several neurodegenerative diseases, such as Parkinson’s, Huntington’s and Alzheimer’s disease (AD). AD is the most common cause of dementia in the elderly and it is characterized by progressive memory loss and cognitive decline along with synaptic dysfunction. Accumulations of amyloid β (Aβ) and tau proteins are two major neuropathological hallmarks of AD. In addition, accumulation of autophagic vacuoles and other autophagic pathology are evident in dystrophic neurites of AD brains. A series of studies has suggested that autophagy is involved in metabolism of Aβ and tau. Moreover, presenilin (PS), a core subunit of γ- secretase complex, has been demonstrated to play an important role in autophagy at the level of lysosomal proteolysis. In spite of several therapeutic approaches through modulation of autophagic pathway, inconsistent results among studies have made it difficult to determine whether autophagy induction will be beneficial or detrimental for AD pathogenesis. Therefore, roles of autophagy in AD need to be further investigated to develop therapeutic strategies in the future.
Keywords: Autophagy, mTOR, rapamycin, beclin, Alzheimer’s disease.
Current Enzyme Inhibition
Title:Role of Autophagy in Alzheimer’s Disease
Volume: 9 Issue: 1
Author(s): Jaekwang Kim, Hyejin Yoon and Jungsu Kim
Affiliation:
Keywords: Autophagy, mTOR, rapamycin, beclin, Alzheimer’s disease.
Abstract: Autophagy is a tightly regulated lysosomal degradation/recycling pathway, critical for cellular homeostasis, such as neuronal survival and death. Impaired autophagic function has been reported in several neurodegenerative diseases, such as Parkinson’s, Huntington’s and Alzheimer’s disease (AD). AD is the most common cause of dementia in the elderly and it is characterized by progressive memory loss and cognitive decline along with synaptic dysfunction. Accumulations of amyloid β (Aβ) and tau proteins are two major neuropathological hallmarks of AD. In addition, accumulation of autophagic vacuoles and other autophagic pathology are evident in dystrophic neurites of AD brains. A series of studies has suggested that autophagy is involved in metabolism of Aβ and tau. Moreover, presenilin (PS), a core subunit of γ- secretase complex, has been demonstrated to play an important role in autophagy at the level of lysosomal proteolysis. In spite of several therapeutic approaches through modulation of autophagic pathway, inconsistent results among studies have made it difficult to determine whether autophagy induction will be beneficial or detrimental for AD pathogenesis. Therefore, roles of autophagy in AD need to be further investigated to develop therapeutic strategies in the future.
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Cite this article as:
Kim Jaekwang, Yoon Hyejin and Kim Jungsu, Role of Autophagy in Alzheimer’s Disease, Current Enzyme Inhibition 2013; 9 (1) . https://dx.doi.org/10.2174/1573408011309010008
DOI https://dx.doi.org/10.2174/1573408011309010008 |
Print ISSN 1573-4080 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6662 |
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