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Cited by 106Alzheimer's disease research and treatmentsCellular transport and secretionNeuroinflammation and Neurodegeneration Mechanisms

Modulation of beta-amyloid precursor protein trafficking and processing by the low density lipoprotein receptor family

Open access
Cam·2006·Molecular Neurodegeneration
DOI 10.1186/1750-1326-1-8PMC PMC1563464
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Abstract

Amyloid-beta peptide (Abeta) accumulation in the brain is an early, toxic event in the pathogenesis of Alzheimer's disease (AD). Abeta is produced by proteolytic processing of a transmembrane protein, beta-amyloid precursor protein (APP), by beta- and gamma-secretases. Mounting evidence has demonstrated that alterations in APP cellular trafficking and localization directly impact its processing to Abeta. Recent studies have shown that members of the low-density lipoprotein receptor family, including LRP, LRP1B, SorLA/LR11, and apolipoprotein E (apoE) receptor 2, interact with APP and regulate its endocytic trafficking. Another common feature of these receptors is their ability to bind apoE, which exists in three isoforms in humans and the presence of the epsilon4 allele represents a genetic risk factor for AD. In this review, we summarize the current understanding of the function of these apoE receptors with a focus on their role in APP trafficking and processing. Knowledge of the interactions between these distinct low-density lipoprotein receptor family members and APP may ultimately influence future therapies for AD.

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  • The cleavage of APP to Aβ in BACE-containing endosomes is exacerbated by the APOE E4 genotype.

    “APP can be cleaved to Aβ (Fig. 5, magenta) when it is trapped in endosomes that contain β-secretase (BACE)143, a process exacerbated by the APOE E4 genotype144,145.”

    From Stress weakens prefrontal networks: molecular insults to higher cognition (2015) · cites this paper as [144]

    The ‘Endocytic trafficking of APP’ section says internalized APP is cleaved by BACE in endosomes and subsequently processed to produce Aβ. The ‘Interaction between LRP and APP’ section reports that applying ApoE4 to cells increased APP endocytosis and Aβ levels, but says it is unclear how ApoE4 influences APP processing; it does not establish that the APOE E4 genotype specifically exacerbates endosomal BACE cleavage. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • The potential role of LDLR on AD pathogenesis has been unclear.

    “Although the effects of LRP1 on Aβ clearance and APP processing have been extensively studied (Cam and Bu, 2006), the potential role of LDLR on AD pathogenesis has been unclear.”

    From Overexpression of Low-Density Lipoprotein Receptor in the Brain Markedly Inhibits Amyloid Deposition and Increases Extracellular Aβ Clearance (2009) · cites this paper as Cam and Bu, 2006

  • LRP1 has been proposed to affect pathogenesis of AD by regulating Aβ catabolism and APP processing.

    “LRP1 has been proposed to affect pathogenesis of AD by regulating Aβ catabolism and APP processing (Cam and Bu, 2006).”

    From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Cam and Bu, 2006

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Authors
Cam
Venue
Molecular Neurodegeneration
Publisher
Springer Science and Business Media LLC
Published
2006
Volume
1
Issue
1
Pages
8
ISSN
1750-1326 (ISSN-L)
DOI
10.1186/1750-1326-1-8
PMC
PMC1563464
OpenAlex
W2115922577
Cited by
106
References
113
Citations by year
2026: 3 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 7 · 2014: 6 · 2013: 4 · 2012: 14
FWCI
7.53
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Molecular Neurodegeneration (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
Funders
  • Alzheimer's Association
  • American Health Assistance Foundation
  • National Institutes of Health
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
amyloid precursor protein, amyloid-beta, Alzheimer's disease, low-density lipoprotein receptor family, LRP, LRP1B, ApoER2, apolipoprotein E, APP trafficking, APP processing, endosomal trafficking, beta-secretase, gamma-secretase, APOE ε4

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