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Dysregulation of protein trafficking in neurodegeneration

Overview of attention for article published in Molecular Neurodegeneration, August 2014
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Title
Dysregulation of protein trafficking in neurodegeneration
Published in
Molecular Neurodegeneration, August 2014
DOI 10.1186/1750-1326-9-31
Pubmed ID
Authors

Xin Wang, Timothy Huang, Guojun Bu, Huaxi Xu

Abstract

Intracellular protein trafficking plays an important role in neuronal function and survival. Protein misfolding is a common theme found in many neurodegenerative diseases, and intracellular trafficking machinery contributes to the pathological accumulation and clearance of misfolded proteins. Although neurodegenerative diseases exhibit distinct pathological features, abnormal endocytic trafficking is apparent in several neurodegenerative diseases, such as Alzheimer's disease (AD), Down syndrome (DS) and Parkinson's disease (PD). In this review, we will focus on protein sorting defects in three major neurodegenerative diseases, including AD, DS and PD. An important pathological feature of AD is the presence of extracellular senile plaques in the brain. Senile plaques are composed of β-amyloid (Aβ) peptide aggregates. Multiple lines of evidence demonstrate that over-production/aggregation of Aβ in the brain is a primary cause of AD and attenuation of Aβ generation has become a topic of extreme interest in AD research. Aβ is generated from β-amyloid precursor protein (APP) through sequential cleavage by β-secretase and the γ-secretase complex. Alternatively, APP can be cleaved by α-secretase within the Aβ domain to release soluble APPα which precludes Aβ generation. DS patients display a strikingly similar pathology to AD patients, including the generation of neuronal amyloid plaques. Moreover, all DS patients develop an AD-like neuropathology by their 40 s. Therefore, understanding the metabolism/processing of APP and how these underlying mechanisms may be pathologically compromised is crucial for future AD and DS therapeutic strategies. Evidence accumulated thus far reveals that synaptic vesicle regulation, endocytic trafficking, and lysosome-mediated autophagy are involved in increased susceptibility to PD. Here we review current knowledge of endosomal trafficking regulation in AD, DS and PD.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 163 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 3 2%
United Kingdom 1 <1%
Unknown 159 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 44 27%
Student > Bachelor 28 17%
Researcher 18 11%
Student > Master 13 8%
Other 8 5%
Other 16 10%
Unknown 36 22%
Readers by discipline Count As %
Agricultural and Biological Sciences 38 23%
Biochemistry, Genetics and Molecular Biology 29 18%
Neuroscience 20 12%
Medicine and Dentistry 12 7%
Immunology and Microbiology 4 2%
Other 17 10%
Unknown 43 26%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 26 August 2014.
All research outputs
#18,376,927
of 22,761,738 outputs
Outputs from Molecular Neurodegeneration
#784
of 846 outputs
Outputs of similar age
#168,132
of 235,902 outputs
Outputs of similar age from Molecular Neurodegeneration
#10
of 10 outputs
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