Protein recycling pathways in neurodegenerative diseases

被引：25

作者：

Fecto, Faisal ^{[1
]}

Esengul, Y. Taylan ^{[1
]}

Siddique, Teepu ^{[1
,2
]}

机构：

[1] Northwestern Univ, Feinberg Sch Med, Davee Dept Neurol & Clin Neurosci, Div Neuromuscular Med, Chicago, IL 60611 USA

[2] Northwestern Univ, Interdept Neurosci Program, Chicago, IL 60611 USA

来源：

ALZHEIMERS RESEARCH & THERAPY | 2014年 / 6卷 / 02期

关键词：

AMYOTROPHIC-LATERAL-SCLEROSIS; UBIQUITIN-PROTEASOME SYSTEM; FRONTOTEMPORAL LOBAR DEGENERATION; ALPHA-SYNUCLEIN; MOUSE MODEL; ALZHEIMERS-DISEASE; MAMMALIAN TARGET; AMYLOID-BETA; PINK1/PARKIN-MEDIATED MITOPHAGY; LYSOSOMAL DYSFUNCTION;

D O I：

10.1186/alzrt243

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Many progressive neurodegenerative diseases, including Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, and frontotemporal lobe dementia, are associated with the formation of insoluble intracellular proteinaceous inclusions. It is therefore imperative to understand the factors that regulate normal, as well as abnormal, protein recycling in neurons. Dysfunction of the ubiquitin-proteasome or autophagy pathways might contribute to the pathology of various neurodegenerative diseases. Induction of these pathways may offer a rational therapeutic strategy for a number of these diseases.

引用

页数：9

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