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Aberrant Presenilin-1 Expression Downregulates LDL Receptor-Related Protein (LRP): Is LRP Central to Alzheimer's Disease Pathogenesis?

Van Uden, Emily, Carlson, George, St. George-Hyslop, Peter, Westaway, David, Orlando, Robert, Mallory, Margaret, Rockenstein, Edward, Masliah, Eliezer·1999·Molecular and Cellular Neuroscience
DOI 10.1006/mcne.1999.0772
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Abstract

Low density lipoprotein receptor-related protein (LRP) polymorphisms have recently been associated with an increased susceptibility of Alzheimer's disease (AD). Furthermore, LRP has been linked to molecules that confer susceptibility to AD (apolipoprotein E, alpha-2-macroglobulin, amyloid precursor protein), previously with the exception of the presenilins. Here we report that aberrant presenilin-1 expression in vivo and in vitro downregulates LRP. Specifically, transgenic mice overexpressing the M146L or L286V presenilin-1 mutation show decreased levels of LRP expression in neuronal populations where presenilin-1 and LRP are closely colocalized or coexpressed. Moreover, cell lines transfected with presenilin-1 also expressed decreased levels of LRP. These findings suggest that LRP may be central to AD pathogenesis since all proteins genetically associated with AD can now be linked via a single pathway to LRP.

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  • It appears that expression of PS1dE9 is implicated in the poor survival of RAP(−/−) mice that harbor the APPswe/PS1dE9 transgene.

    “At present the basis for poor survival is unknown but it appears that expression of PS1dE9 is implicated because others have not noted that expression of mutant APP in a RAP null background decreases survival [27].”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [27]

  • Expression of PS1 variants M146L or L286V, which are linked to familial AD, cause 40% reductions in the levels of mature LRP in brain.

    “It is noteworthy that expression of PS1 variants M146L or L286V, which are linked to familial AD, also cause 40% reductions in the levels of mature LRP in brain [27].”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [27]

  • The levels of mature, endoproteolytically cleaved, LRP in the murine nervous system are reduced when AD associated mutants of PS1 (M146L or L286V, expressed via the hamster prion protein gene promoter) are present.

    “It has been reported that the levels of mature, endoproteolytically cleaved, LRP in the murine nervous system are reduced when AD associated mutants of PS1 (M146L or L286V, expressed via the hamster prion protein gene promoter) are present [27].”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [27]

  • Reductions in LRP and/or SorLA/LR11 that are of a significantly greater magnitude than found here produce significant changes in amyloidogenesis.

    “Collectively, these studies suggest that reductions in LRP and/or SorLA/LR11 that are of a significantly greater magnitude than found here produce significant changes in amyloidogenesis.”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [27]

  • In Van Uden et al. study of PDGF-APPInd mice mated to RAP KO mice, increases in amyloid burden were correlated with 80% reductions in the levels of mature LRP.

    “In the study by Van Uden and colleagues of PDGF-APPInd mice mated to RAP KO mice, increases in amyloid burden were correlated with 80% reductions in the levels of mature LRP [27].”

    From Receptor-Associated Protein (RAP) Plays a Central Role in Modulating Aβ Deposition in APP/PS1 Transgenic Mice (2008) · cites this paper as [27]

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Metadata

Authors
Van Uden, E., Carlson, G., St. George-Hyslop, P., Westaway, D., Orlando, R., Mallory, M., Rockenstein, E., & Masliah, E.
Venue
Molecular and Cellular Neuroscience
Publisher
Elsevier BV
Published
1999-08
Volume
14
Issue
2
Pages
129-140
ISSN
1044-7431
DOI
10.1006/mcne.1999.0772
Cited by
32
References
7
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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