ArticlePathobiology of aging & age related diseases2015
LINGO-1 promotes lysosomal degradation of amyloid-β protein precursor.
Article in Pathobiology of aging & age related diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Multi-ancestry exome-wide study identifies variants associated with Alzheimer's disease protection.Journal of Alzheimer's disease : JAD · 2026Article
- Molecular hallmarks of excitatory and inhibitory neuronal resilience to Alzheimer's disease.Molecular neurodegeneration · 2025Article
- Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Revealing age-related changes in the intraocular microenvironment and senescence modulators using aqueous humor proteomics and machine learning.Frontiers in cell and developmental biology · 2025Article
- Genome-wide association neural networks identify genes linked to family history of Alzheimer's disease.Briefings in bioinformatics · 2024Article
- Xenografted human iPSC-derived neurons with the familial Alzheimer's disease APPActa neuropathologica · 2024Article
- Small Molecule Drug C381 Attenuates Brain Vascular Damage Following Repetitive Mild Traumatic Injury.Neurotrauma reports · 2024Article
- Nogo-A and LINGO-1: Two Important Targets for Remyelination and Regeneration.International journal of molecular sciences · 2023Review
- Myelin repair in Alzheimer's disease: a review of biological pathways and potential therapeutics.Translational neurodegeneration · 2022Review
- Article
- Endo-lysosomal pathway and ubiquitin-proteasome system dysfunction in Alzheimer's disease pathogenesis.Neuroscience letters · 2019Review
- APP Receptor? To Be or Not To Be.Trends in pharmacological sciences · 2016Review
- Intracellular LINGO-1 negatively regulates Trk neurotrophin receptor signaling.Molecular and cellular neurosciences · 2016Article
- Lingo-1: a novel target in therapy for Alzheimer's disease?Neural regeneration research · 2016Article
- Altered gene expression in excitatory neurons is associated with Alzheimer's disease and its higher incidence in women.Alzheimer's & dementia (New York, N. Y.)Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Sequential proteolytic cleavages of amyloid-β protein precursor (AβPP) by β-secretase and γ-secretase generate amyloid β (Aβ) peptides, which are thought to contribute to Alzheimer's disease (AD). Much of this processing occurs in endosomes following endocytosis of AβPP from the plasma membrane. However, this pathogenic mode of processing AβPP may occur in competition with lysosomal degradation of AβPP, a common fate of membrane proteins trafficking through the endosomal system. Following up on published reports that LINGO-1 binds and promotes the amyloidogenic processing of AβPP we have examined the consequences of LINGO-1/AβPP interactions. We report that LINGO-1 and its paralogs, LINGO-2 and LINGO-3, decrease processing of AβPP in the amyloidogenic pathway by promoting lysosomal degradation of AβPP. We also report that LINGO-1 levels are reduced in AD brain, representing a possible pathogenic mechanism stimulating the generation of Aβ peptides in AD.
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