The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
The Role of SORL1 in Alzheimer’s Disease
Abstract
Genetic variation in SORL1 gene, also known as LR11, has been identified to associate with Alzheimer's disease (AD) through replicated genetic studies. As a type I transmembrane protein, SORL1 is composed of several distinct domains and belongs to both the low-density lipoprotein receptor (LDLR) family and the vacuolar protein sorting 10 (VPS10) domain receptor family. The level of SORL1 was found to be decreased in the AD brain which positively correlated with β-amyloid (Aβ) accumulation. Emerging data suggests that SORL1 contributes to AD through various pathways, including emerging as a central regulator of the trafficking and processing of amyloid precursor protein (APP), involvement in Aβ destruction, and interaction with ApoE and tau protein. Primarily, SORL1 interacts with distinct sets of cytosolic adaptors for anterograde and retrograde movement of APP between the trans-Golgi network (TGN) and early endosomes, thereby restricting the delivery of the precursor to endocytic compartments that favor amyloidogenic breakdown. In this article, we review recent epidemiological and genetical findings of SORL1 that related with AD and speculate the possible roles of SORL1 in the progression of this disease. Finally, given the potential contributions of SORL1 to AD pathogenesis, targeting SORL1 might present novel opportunities for AD therapy.
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“SORL1 underexpression has also been associated with an increase in Aβ production by blocking the redirection of endocytosed APP to the trans-Golgi network, which reduces APP processing in endosomes [113, 144, 152].”
From The new genetic landscape of Alzheimer’s disease: from amyloid cascade to genetically driven synaptic failure hypothesis? (2019) · cites this paper as [152]
In the citing paper
“SORLA is involved in APP processing, Aβ secretion and Aβ turnover [484].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [484]
Citations
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Metadata
- Authors
- Yin, R.-H., Yu, J.-T., & Tan, L.
- Affiliations
- Qingdao University (CN)
- Corresponding author
- Tan, Lan
- ORCID
- Venue
- Molecular Neurobiology
- Published
- 2014-05-16
- Volume
- 51
- Issue
- 3
- Pages
- 909-918
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W2064885915
- Cited by
- 126
- References
- 61
- Citations by year
- 2026: 13 · 2025: 9 · 2024: 17 · 2023: 15 · 2022: 8 · 2021: 13 · 2020: 15 · 2019: 9 · 2018: 8 · 2017: 4 · 2016: 7 · 2015: 4 · 2014: 4
- FWCI
- 0.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- SORL1, Alzheimer's disease, genetic association, amyloid precursor protein, amyloid-beta, APP trafficking, apolipoprotein E, tau protein, trans-Golgi network, early endosomes, amyloidogenic processing, disease progression, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Humans, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, LDL-Receptor Related Proteins, Membrane Transport Proteins, Amyloid Precursor Protein Secretases
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