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Loss of LR11/SORLA Enhances Early Pathology in a Mouse Model of Amyloidosis: Evidence for a Proximal Role in Alzheimer's Disease
Open accessAbstract
Alzheimer's disease (AD) is the most prevalent form of dementia, resulting in progressive neuronal death and debilitating damage to brain loci that mediate memory and higher cognitive function. While pathogenic genetic mutations have been implicated in ∼2% of AD cases, the proximal events that underlie the common, sporadic form of the disease are incompletely understood. Converging lines of evidence from human neuropathology, basic biology, and genetics have implicated loss of the multifunctional receptor LR11 (also known as SORLA and SORL1) in AD pathogenesis. Cell-based studies suggest that LR11 reduces the formation of β-amyloid (Aβ), the molecule believed to be a primary toxic species in AD. Recently, mutant mice deficient in LR11 were shown to upregulate murine Aβ in mouse brain. In the current study, LR11-deficient mice were crossed with transgenic mice expressing autosomal-dominant human AD genes, presenilin-1 (PS1ΔE9) and amyloid precursor protein (APPswe). Here, we show that LR11 deficiency in this AD mouse model significantly increases Aβ levels and exacerbates early amyloid pathology in brain, causing a forward shift in disease onset that is LR11 gene dose-dependent. Loss of LR11 increases the processing of the APP holo-molecule into α-, β-, and γ-secretase derived metabolites. We propose that LR11 regulates APP processing and Aβ accumulation in vivo and is of proximal importance to the cascade of pathological amyloidosis. The results of the current study support the hypothesis that control of LR11 expression may exert critical effects on Alzheimer's disease susceptibility in humans.
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“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 [16]
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“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 [16]
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“Consistent with the previous cell-based studies, reduction of LR11/SorLA protein levels increased Aβ levels and exacerbated amyloid plaque pathology in an APP/PSEN1Δ9 mouse model of amyloidosis (Dodson et al., 2008).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Dodson et al., 2008
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“Overexpression of SORLA in neuronal cells can block amyloidogenic processing and reduce Aβ production [485], whereas loss of SORLA increased extracellular Aβ levels and plaque deposition in several AD mouse models [486, 487].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [487]
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Metadata
- Authors
- Dodson, S. E., Andersen, O. M., Karmali, V., Fritz, J. J., Cheng, D., Peng, J., Levey, A. I., Willnow, T. E., & Lah, J. J.
- Affiliations
- Emory University (US)
- Aarhus University (DK)
- Max Delbrück Center (DE)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-11-26
- Volume
- 28
- Issue
- 48
- Pages
- 12877-12886
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC2669320
- OpenAlex
- W1967519462
- Cited by
- 141
- References
- 44
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 8 · 2022: 8 · 2021: 9 · 2020: 7 · 2019: 7 · 2018: 9 · 2017: 7 · 2016: 9 · 2015: 12 · 2014: 10 · 2013: 8 · 2012: 12
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- Journal of Neuroscience Nursing
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health (AG05136)
- National Institute on Aging (R01AG024214, AG 05136, P50AG005136)
- National Institute of Neurological Disorders and Stroke (F31NS055881)
- 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 › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- LR11, SorLA, SORL1, Alzheimer's disease, amyloidosis, amyloid-beta, APP processing, presenilin 1, APPswe, gene dosage, disease onset, transgenic mouse model
- MeSH terms
- Alzheimer Disease, Amyloidosis, Animals, Brain, Disease Models, Animal, Gene Expression Regulation, Humans, Mice, Transgenic, Neurons, Receptors, LDL, Up-Regulation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice, Knockout, Gene Dosage, Genetic Predisposition to Disease, Membrane Transport Proteins, Mice, Plaque, Amyloid
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