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Cited by 89

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Sortilin-related Receptor with A-type Repeats (SORLA) Affects the Amyloid Precursor Protein-dependent Stimulation of ERK Signaling and Adult Neurogenesis

Rohe, Michael, Carlo, Anne-Sophie, Breyhan, Henning, Sporbert, Anje, Militz, Daniel, Schmidt, Vanessa, Wozny, Christian, Harmeier, Anja, Erdmann, Bettina, Bales, Kelly R., Wolf, Susanne, Kempermann, Gerd, Paul, Steven M., Schmitz, Dietmar, Bayer, Thomas A., Willnow, Thomas E., Andersen, Olav M.·2008·Journal of Biological Chemistry
DOI 10.1074/jbc.m710574200
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Crossref · 10.1074/jbc.m710574200

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  • Loss of SORL1 expression in several mouse models of AD increases extracellular Aβ levels.

    “Indeed, loss of SORL1 expression in several mouse models of AD increases extracellular Aβ levels, the aggregation of which triggers AD pathology [15–17].”

    From Impaired SorLA maturation and trafficking as a new mechanism for SORL1 missense variants in Alzheimer disease (2021) · cites this paper as [17]

    The Results report increased Aβ production and a threefold higher plaque burden when SORLA was lost in PDAPP mice; a second SORLA-deficient line on the PDAPP background also showed increased plaques. The paper does not establish increased extracellular Aβ levels across several distinct AD mouse models: its AD experiments use the PDAPP model, and its Aβ measurements are not specified as extracellular. (LLM, conf=0.86)

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  • SorLA deficiency results in increased production of Aβ peptides and thus a higher risk of AD.

    “Functional and genetic studies demonstrated that SorLA deficiency results in increased production of Aβ peptides, and thus a higher risk of AD.”

    From Impaired SorLA maturation and trafficking as a new mechanism for SORL1 missense variants in Alzheimer disease (2021) · cites this paper as [17]

    The Results report increased Aβ40 in SORLA-deficient mice, and the Discussion reports increased amyloid peptide formation across mouse models. The Discussion says these findings support the possibility that insufficient SORLA expression may be a risk factor for human AD; it does not establish that deficiency results in a higher risk in people. Page numbers were not provided in our copy. (LLM, conf=0.88)

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Research works printed but not linked: 36

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Metadata

Authors
Rohe, M., Carlo, A.-S., Breyhan, H., Sporbert, A., Militz, D., Schmidt, V., Wozny, C., Harmeier, A., Erdmann, B., Bales, K. R., Wolf, S., Kempermann, G., Paul, S. M., Schmitz, D., Bayer, T. A., Willnow, T. E., & Andersen, O. M.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2008-05
Volume
283
Issue
21
Pages
14826-14834
ISSN
0021-9258
DOI
10.1074/jbc.m710574200
Cited by
89
References
2
Language
en
Licence

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