Evidence map›Paper›PMID 28381441›Full record

ReviewJournal of lipid research2017

Role of LRP1 in the pathogenesis of Alzheimer's disease: evidence from clinical and preclinical studies.

Mitsuru Shinohara, Masaya Tachibana, Takahisa Kanekiyo, Guojun Bu

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

192 citing papers in PubMed, 1 synthesis or guideline pooled it, 284 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Article
  6. International journal of molecular sciences · 2026
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  13. Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  14. Article
  15. Review
  16. Article
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132 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Mitsuru ShinoharaDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL. Electronic address: shinohara@ncgg.go.jp.
Masaya TachibanaDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL.
Takahisa KanekiyoDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL.
Guojun BuDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL.
Mayo Clinic in Florida · US

Funding

THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI PETERSEN, RONALD C · 1999 to 2018
$36.9M
Viral Vectors CoreP01NS074969 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2012 to 2021
$13.0M
Integrative translational discovery of vascular risk factors in aging and dementiaRF1AG051504 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN, ERTEKIN-TANER, NILUFER · 2015 to 2019
$9.8M
ApoE Receptor Pathways to Intraneuronal AbetaR01AG027924 · NIA · WASHINGTON UNIVERSITY · PI LI, YONGHE · 2006 to 2021
$3.7M
BRAIN LIPID METABOLISM, DENDRITES AND SYNAPSES IN AGING AND ALZHEIMER'S DISEASER01AG035355 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2010 to 2019
$3.1M
ApoE isoform-specific therapy for Alzheimer diseaseR01AG046205 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2013 to 2017
$1.6M
NIA NIH HHS P50 AG016574NIA NIH HHS R01 AG027924NIA NIH HHS R01 AG035355NIA NIH HHS R01 AG046205NIA NIH HHS RF1 AG051504NINDS NIH HHS P01 NS074969
6 · The paper itself

Abstract

Among the LDL receptor (LDLR) family members, the roles of LDLR-related protein (LRP)1 in the pathogenesis of Alzheimer's disease (AD), especially late-onset AD, have been the most studied by genetic, neuropathological, and biomarker analyses (clinical studies) or cellular and animal model systems (preclinical studies) over the last 25 years. Although there are some conflicting reports, accumulating evidence from preclinical studies indicates that LRP1 not only regulates the metabolism of amyloid-β peptides (Aβs) in the brain and periphery, but also maintains brain homeostasis, impairment of which likely contributes to AD development in Aβ-independent manners. Several preclinical studies have also demonstrated an involvement of LRP1 in regulating the pathogenic role of apoE, whose gene is the strongest genetic risk factor for AD. Nonetheless, evidence from clinical studies is not sufficient to conclude how LRP1 contributes to AD development. Thus, despite very promising results from preclinical studies, the role of LRP1 in AD pathogenesis remains to be further clarified. In this review, we discuss the potential mechanisms underlying how LRP1 affects AD pathogenesis through Aβ-dependent and -independent pathways by reviewing both clinical and preclinical studies. We also discuss potential therapeutic strategies for AD by targeting LRP1.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EBiomarkersHumansLow Density Lipoprotein Receptor-Related Protein-1Molecular Targeted TherapyAmyloid beta-PeptidesApolipoproteins EBiomarkersLow Density Lipoprotein Receptor-Related Protein-1gene expressionlow density lipoprotein receptor-related protein 1receptors/lipoproteintransport

Identifiers

PMID28381441
PMCPMC5496044
OpenAlexW2605039207

What OpenQuestion holds

Textmetadata
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.