ArticleThe Journal of clinical investigation2013
Endocytosis of synaptic ADAM10 in neuronal plasticity and Alzheimer's disease.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 113 citations in OpenAlex.
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- Neuropathy-associated Tecpr2 mutation knock-in mice reveal endolysosomal loss of function phenotypes in neurons and microglia.Cell death & disease · 2025Article
- Peripheral Choroid/RPE/Sclera as a Shared Pathogenic Hub: Multi-Tissue Transcriptomic Profiling Identifies Common Differentially Expressed Genes in Age-Related Macular Degeneration and Alzheimer's Disease.Molecular neurobiology · 2025Article
- GALM Alleviates Aβ Pathology and Cognitive Deficit Through Increasing ADAM10 Maturation in a Mouse Model of Alzheimer's Disease.Neuroscience bulletin · 2025Article
- Peptide Fraction fromAntioxidants (Basel, Switzerland) · 2025Article
- A Valuable Target for Therapy: The Metalloproteinase ADAM10.Current protein & peptide science · 2025Review
- Cholesterol and Lipid Rafts in the Biogenesis of Amyloid-β Protein and Alzheimer's Disease.Annual review of biophysics · 2024Review
- Comprehensive Overview of Alzheimer's Disease: Etiological Insights and Degradation Strategies.International journal of molecular sciences · 2024Review
- Deciphering the Role of Peroxisome Proliferator-activated Receptor α and Phosphodiesterase Type 5 Targets in Alzheimer's Disease.CNS & neurological disorders drug targets · 2024Review
- Novel therapeutic approaches to target neurodegeneration.British journal of pharmacology · 2023Review
- Tip60's Novel RNA-Binding Function Modulates Alternative Splicing of Pre-mRNA Targets Implicated in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Therapeutic potential of ADAM10 modulation in Alzheimer's disease: a review of the current evidence.Cell communication and signaling : CCS · 2023Review
- Treadmill workout activates PPARα in the hippocampus to upregulate ADAM10, decrease plaques and improve cognitive functions in 5XFAD mouse model of Alzheimer's disease.Brain, behavior, and immunity · 2023Article
- A Bioengineering Strategy to Control ADAM10 Activity in Living Cells.International journal of molecular sciences · 2023Article
- Shifting the balance: soluble ADAM10 as a potential treatment for Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Ectodomain shedding of EGFR ligands serves as an activation readout for TRP channels.PloS one · 2023Article
- The development of ADAM10 endocytosis inhibitors for the treatment of Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Rabphilin-3A Drives Structural Modifications of Dendritic Spines Induced by Long-Term Potentiation.Cells · 2022Article
- An unexpected role for the conserved ADAM-family metalloprotease ADM-2 in Caenorhabditis elegans molting.PLoS genetics · 2022Article
- Analysis of mRNA and Protein Levels ofInternational journal of molecular sciences · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A disintegrin and metalloproteinase 10 (ADAM10), a disintegrin and metalloproteinase that resides in the postsynaptic densities (PSDs) of excitatory synapses, has previously been shown to limit β-amyloid peptide (Aβ) formation in Alzheimer's disease (AD). ADAM10 also plays a critical role in regulating functional membrane proteins at the synapse. Using human hippocampal homogenates, we found that ADAM10 removal from the plasma membrane was mediated by clathrin-dependent endocytosis. Additionally, we identified the clathrin adaptor AP2 as an interacting partner of a previously uncharacterized atypical binding motif in the ADAM10 C-terminal domain. This domain was required for ADAM10 endocytosis and modulation of its plasma membrane levels. We found that the ADAM10/AP2 association was increased in the hippocampi of AD patients compared with healthy controls. Long-term potentiation (LTP) in hippocampal neuronal cultures induced ADAM10 endocytosis through AP2 association and decreased surface ADAM10 levels and activity. Conversely, long-term depression (LTD) promoted ADAM10 synaptic membrane insertion and stimulated its activity. ADAM10 interaction with the synapse-associated protein-97 (SAP97) was necessary for LTD-induced ADAM10 trafficking and required for LTD maintenance and LTD-induced changes in spine morphogenesis. These data identify and characterize a mechanism controlling ADAM10 localization and activity at excitatory synapses that is relevant to AD pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.