자가포식현상과 신경퇴행병 (Autophagy and Neurodegenerative Diseases)

서지정보

· 발행기관 : 대한신경과학회
· 수록지 정보 : 대한신경과학회지 / 27권 / 3호 / 206 ~ 214페이지
· 저자명 : 백진영, 김범생

초록

Autophagy is a highly regulated cellular mechanism that results in the bulk degradation of long-lived proteins and
organelles and which seems to be implicated in a variety of physiological and pathological conditions relevant to
neurological diseases. The formation of intraneuronal mutant protein aggregates is a characteristic of several human
neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, and polyglutamine disorders such as
Huntington’s disease (HD). Autophagy is a major clearance pathway for the removal of the mutant huntingtin protein
associated with HD, and many other disease-causing, cytoplasmic, aggregate-prone proteins. Autophagy is negatively
regulated by the mammalian target of rapamycin (mTOR) and can be induced in all mammalian cell types by the mTOR
inhibitor rapamycin. It can also be induced by an mTOR-independent pathway, which has multiple drug targets,
involving links between Ca2+-calpain–Gsα and cAMP–Epac–PLC-e–IP3 signaling. Both pathways enhance the process of
autophagy. In this review, we describe the various drugs and pathways that induce autophagy that are potential
therapeutic approaches for neurodegenerative disorders.

영어초록

Autophagy is a highly regulated cellular mechanism that results in the bulk degradation of long-lived proteins and
organelles and which seems to be implicated in a variety of physiological and pathological conditions relevant to
neurological diseases. The formation of intraneuronal mutant protein aggregates is a characteristic of several human
neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, and polyglutamine disorders such as
Huntington’s disease (HD). Autophagy is a major clearance pathway for the removal of the mutant huntingtin protein
associated with HD, and many other disease-causing, cytoplasmic, aggregate-prone proteins. Autophagy is negatively
regulated by the mammalian target of rapamycin (mTOR) and can be induced in all mammalian cell types by the mTOR
inhibitor rapamycin. It can also be induced by an mTOR-independent pathway, which has multiple drug targets,
involving links between Ca2+-calpain–Gsα and cAMP–Epac–PLC-e–IP3 signaling. Both pathways enhance the process of
autophagy. In this review, we describe the various drugs and pathways that induce autophagy that are potential
therapeutic approaches for neurodegenerative disorders.

참고자료

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