LRP in Alzheimer's disease: friend or foe? - PubMed (original) (raw)

Review

LRP in Alzheimer's disease: friend or foe?

P G Ulery et al. J Clin Invest. 2000 Nov.

No abstract available

PubMed Disclaimer

Figures

Figure 1

Figure 1

Proposed dual role of LRP in Aβ metabolism. Association of Aβ with LRP ligands (apoE, α2M*, or lactoferrin) results in rapid LRP-mediated endocytosis of the complex. On the other hand, association of APP isoforms containing KPI domains (APPKPI) leads to increased Aβ generation and deposition. In AD, the catabolic pathway may be impaired by decreased levels of LRP at clearance sites (perhaps neurons or sites along the capillary membranes), while Aβ generation may be enhanced by upregulation of LRP in activated glia found in the AD brain.

Similar articles

Cited by

References

    1. Tanzi RE, et al. The amyloid β protein gene: cDNA cloning, mRNA distribution, and genetic linkage near the Alzheimer locus. Science. 1987;235:880–994. - PubMed
    1. Brown MS, Ye J, Rawson RB, Goldstein JL. Regulated intramembrane proteolysis: a control mechanism conserved from bacteria to humans. Cell. 2000;100:391–398. - PubMed
    1. Vassar R, et al. Beta-secretase cleavage of Alzheimer’s amyloid precursor protein by the transmembrane aspartic protease BACE. Science. 1999;286:735–741. - PubMed
    1. Li YM, et al. Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1. Nature. 2000;405:689–694. - PubMed
    1. St. George-Hyslop PH, et al. The genetic defect causing familial Alzheimer’s disease maps on chromosome 21. Science. 1987;235:885–890. - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources