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Soluble apoE/Aβ complex: mechanism and therapeutic target for APOE4-induced AD risk

Overview of attention for article published in Molecular Neurodegeneration, January 2014
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Title
Soluble apoE/Aβ complex: mechanism and therapeutic target for APOE4-induced AD risk
Published in
Molecular Neurodegeneration, January 2014
DOI 10.1186/1750-1326-9-2
Pubmed ID
Authors

Leon M Tai, Shipra Mehra, Varsha Shete, Steve Estus, G William Rebeck, Guojun Bu, Mary Jo LaDu

Abstract

The APOE4 allele of apolipoprotein E (apoE) is the greatest genetic risk factor for Alzheimer's disease (AD) compared to APOE2 and APOE3. Amyloid-β (Aβ), particularly in a soluble oligomeric form (oAβ), is considered a proximal cause of neurodegeneration in AD. Emerging data indicate that levels of soluble oAβ are increased with APOE4, providing a potential mechanism of APOE4-induced AD risk. However, the pathway(s) by which apoE4 may increase oAβ levels are unclear and the subject of continued inquiry. In this editorial review, we present the hypothesis that apoE isoform-specific interactions with Aβ, namely apoE/Aβ complex, modulate Aβ levels. Specifically, we propose that compared to apoE3, apoE4-containing lipoproteins are less lipidated, leading to less stable apoE4/Aβ complexes, resulting in reduced apoE4/Aβ levels and increased accumulation, particularly of oAβ. Evidence that support or counter this argument, as well as the therapeutic significance of this pathway to neurodegeneration, are discussed.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 142 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 <1%
Italy 1 <1%
Unknown 140 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 37 26%
Researcher 24 17%
Student > Master 19 13%
Student > Bachelor 17 12%
Student > Doctoral Student 10 7%
Other 22 15%
Unknown 13 9%
Readers by discipline Count As %
Agricultural and Biological Sciences 44 31%
Neuroscience 26 18%
Chemistry 12 8%
Biochemistry, Genetics and Molecular Biology 11 8%
Medicine and Dentistry 10 7%
Other 21 15%
Unknown 18 13%

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 14 September 2014.
All research outputs
#17,713,929
of 22,745,803 outputs
Outputs from Molecular Neurodegeneration
#760
of 845 outputs
Outputs of similar age
#220,587
of 304,903 outputs
Outputs of similar age from Molecular Neurodegeneration
#18
of 20 outputs
Altmetric has tracked 22,745,803 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 845 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 14.1. This one is in the 7th percentile – i.e., 7% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 304,903 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 24th percentile – i.e., 24% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 20 others from the same source and published within six weeks on either side of this one. This one is in the 10th percentile – i.e., 10% of its contemporaries scored the same or lower than it.