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Low Density Lipoprotein Receptor-Related Proteins (LRPs), Alzheimers and Cognition

Harris-White, M., Frautschy, S.·2005·Current Drug Target -CNS & Neurological Disorders
DOI 10.2174/156800705774322102
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Abstract

This review will focus primarily on the role of the low density lipoprotein receptor-related protein (LRP-1) in neuronal synapse formation and function in Alzheimer's Disease (AD). We review the role that its ligands may have in cognition or AD: apolipoprotein E (ApoE), alpha2-macroglobulin, Transforming Growth Factor-Beta (TGFbeta, Tissue Plasminogen Activator (tPA), insulin growth factor binding protein-3 (IGFBP-3), which all bind LRP-1 and apolipoprotein J (ApoJ), which is a ligand for LRP-2. After reviewing its role as a signaling receptor, we discuss the connection between LRP and the NMDA glutamate receptor via the post synaptic density 95 (PSD-95) neuronal scaffold protein and the implications it may have for memory and cognition. Finally, we discuss the evidence supporting a role for LRP in AD. Although the evidence for LRP as a genetic risk factor is weak, many of its ligands impose genetic risk, and have been implicated in AD pathogenic cascades. We discuss the role of LRP in amyloid precursor protein (APP) processing and production of beta-amyloid (Abeta. We identify LRP ligands that accelerate aggregation of toxic Abeta species. LRP mediates crucial pathways in AD pathogenesis such as Abeta clearance, Abeta uptake, intraneuronal Abeta accumulation and Abeta-associated neuron death. Interestingly, the TGFbeta -V receptor is LRP-1. Data show that one critical ligand TGFbeta2, associated with neurodegeneration in amyloid diseases, induces LRP expression in PC12 cells…

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  • The LDLR family is implicated in the breakdown of synaptic function in Alzheimer's disease.

    “The LDLR family has also been implicated in the breakdown of synaptic function in AD [6].”

    From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [6]

  • In patients with FH, it is very common for the LDLRs that participate in synapse maintenance to be dysfunctional, a pathogenic sign of AD.

    “Moreover, in patients with FH, it is very common for the LDLRs that participate in synapse maintenance to be dysfunctional, a pathogenic sign of AD [6].”

    From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [6]

  • LRP1 is a plasma membrane receptor mediating endocytosis, phagocytosis, chemotaxis and signaling for extracellular ligands including ApoE, lipoproteins, α2-macroglobulin, proteases, extracellular matrix proteins, growth factors, complement factors, heat shock proteins and dozens of other natural ligands.

    “Low density lipoprotein (LDL) receptor related protein 1 (LRP1) is a plasma membrane receptor mediating endocytosis, phagocytosis, chemotaxis and signaling for extracellular ligands, including apolipoprotein E (ApoE), lipoproteins, α2-macroglobulin, proteases, extracellular matrix proteins, growth factors, complement factors, heat shock proteins and dozens of other natural ligands (1–5).”

    From LRPAP1 is released from activated microglia and inhibits microglial phagocytosis and amyloid beta aggregation (2023) · cites this paper as [1]

  • LRP1 and related LDL family receptors regulate a wide range of cellular processes, including endocytosis, phagocytosis, chemotaxis and signaling in response to dozens of ligands.

    “Outside the brain, LRP1 and related LDL family receptors regulate a wide range of cellular processes, including endocytosis, phagocytosis, chemotaxis and signaling in response to dozens of ligands (1–4).”

    From LRPAP1 is released from activated microglia and inhibits microglial phagocytosis and amyloid beta aggregation (2023) · cites this paper as [1]

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Metadata

Authors
Harris-White, M., & Frautschy, S.
Venue
Current Drug Target -CNS & Neurological Disorders
Publisher
Bentham Science Publishers Ltd.
Published
2005-10-01
Volume
4
Issue
5
Pages
469-480
ISSN
1568-007X
DOI
10.2174/156800705774322102
Cited by
58
References
0
Language
en

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