Protein folding and misfolding in the neurodegenerative disorders: A review

被引:27
作者
Boshette, N. B. [1 ]
Thakur, K. K. [1 ]
Bidkar, A. P. [1 ]
Trandafir, C. [3 ]
Kumar, P. [2 ]
Gogoi, R. [1 ]
机构
[1] Gauhati Med Coll, Biotechnol Lab, Dept Biotechnol, Natl Inst Pharmaceut Educ & Res, Gauhati 781032, Assam, India
[2] Gauhati Med Coll, Lab Mol Pharmacol & Toxicol, Dept Pharmacol & Toxicol, Natl Inst Pharmaceut Educ & Res, Gauhati 781032, Assam, India
[3] Univ Med & Pharm Iuliu Hatieganu, Fac Med, Cluj Napoca 400349, Romania
关键词
UBIQUITIN-PROTEASOME PATHWAY; ALZHEIMERS-DISEASE; ALPHA-SYNUCLEIN; AMYLOID-BETA; PARKINSONS-DISEASE; MOLECULAR CHAPERONES; IN-VIVO; NEUROTOXICITY; AGGREGATION; DYNAMICS;
D O I
10.1016/j.neurol.2013.11.002
中图分类号
R74 [神经病学与精神病学];
学科分类号
100204 [神经病学];
摘要
Protein misfolding is an intrinsic aspect of normal folding within the complex cellular environment. Its effects are minimized in living system by the action of a range of protective mechanisms including molecular chaperones and quality control systems. According to the current growing research, protein misfolding is a recognized key feature of most neurodegenerative diseases. Extensive biochemical, neuropathological, and genetic evidence suggest that the cerebral accumulation of amyloid fibrils is the central event in the pathogenesis of neurodegenerative disorders. In the first part of this review we have discussed the general course of action of folding and misfolding of the proteins. Later part of this review gives an outline regarding the role of protein misfolding in the molecular and cellular mechanisms in the pathogenesis of Alzheimer's and Parkinson along with their treatment possibilities. Finally, we have mentioned about the recent findings in neurodegenerative diseases. © 2014 Elsevier Masson SAS.
引用
收藏
页码:151 / 161
页数:11
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