Evidence map›Paper›PMID 28298885›Full record

ReviewFrontiers in molecular neuroscience2017

Functional Roles of the Interaction of APP and Lipoprotein Receptors.

Theresa Pohlkamp, Catherine R Wasser, Joachim Herz

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. LRP10 and α-synuclein transmission in Lewy body diseases.Cellular and molecular life sciences : CMLS · 2024
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Theresa PohlkampDepartment of Molecular Genetics, UT Southwestern Medical CenterDallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical CenterDallas, TX, USA.
Catherine R WasserDepartment of Molecular Genetics, UT Southwestern Medical CenterDallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical CenterDallas, TX, USA.
Joachim HerzDepartment of Molecular Genetics, UT Southwestern Medical CenterDallas, TX, USA; Center for Translational Neurodegeneration Research, UT Southwestern Medical CenterDallas, TX, USA; Department of Neuroscience, UT Southwestern Medical CenterDallas, TX, USA; Department of Neurology and Neurotherapeutics, UT Southwestern Medical CenterDallas, TX, USA.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

Metabolism of the VLDL receptor and ApoE receptor 2R37HL063762 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2010 to 2019
$4.0M
Physiology and Pathophysiology of Apolipoprotein E receptor-2 splicing in Alzheimer's diseaseRF1AG053391 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.4M
Molecular Basis of Synaptic Suppression by ApoER01NS093382 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.0M
NHLBI NIH HHS R37 HL063762NIA NIH HHS RF1 AG053391NINDS NIH HHS R01 NS093382
6 · The paper itself

Abstract

The biological fates of the key initiator of Alzheimer's disease (AD), the amyloid precursor protein (APP), and a family of lipoprotein receptors, the low-density lipoprotein (LDL) receptor-related proteins (LRPs) and their molecular roles in the neurodegenerative disease process are inseparably interwoven. Not only does APP bind tightly to the extracellular domains (ECDs) of several members of the LRP group, their intracellular portions are also connected through scaffolds like the one established by FE65 proteins and through interactions with adaptor proteins such as X11/Mint and Dab1. Moreover, the ECDs of APP and LRPs share common ligands, most notably Reelin, a regulator of neuronal migration during embryonic development and modulator of synaptic transmission in the adult brain, and Agrin, another signaling protein which is essential for the formation and maintenance of the neuromuscular junction (NMJ) and which likely also has critical, though at this time less well defined, roles for the regulation of central synapses. Furthermore, the major independent risk factors for AD, Apolipoprotein (Apo) E and ApoJ/Clusterin, are lipoprotein ligands for LRPs. Receptors and ligands mutually influence their intracellular trafficking and thereby the functions and abilities of neurons and the blood-brain-barrier to turn over and remove the pathological product of APP, the amyloid-β peptide. This article will review and summarize the molecular mechanisms that are shared by APP and LRPs and discuss their relative contributions to AD.

Indexed as

amyloid betaAPOEglutamate receptorsLDL receptor gene familyLRPneuromuscular junctionsynapsetrafficking

Identifiers

PMID28298885
PMCPMC5331069
OpenAlexW2592457424

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.