ArticleEBioMedicine2016
ADAM30 Downregulates APP-Linked Defects Through Cathepsin D Activation in Alzheimer's Disease.
Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
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- Transcriptomic and proteomic insights into progressive myoclonus epilepsy type 1.Disease models & mechanisms · 2026Article
- Presenilin-dependent regulation of neuronal tau pathology via the autophagy and proteasome pathways.Acta neuropathologica communications · 2026Article
- Photocleavable Mass-Tagged Oligonucleotide Probes for Multiplexed and Multiomic Tissue Imaging of Targeted Transcripts.Journal of the American Society for Mass Spectrometry · 2025Article
- Targeted demethylation of cathepsin D via epigenome editing rescues pathology in Alzheimer's disease mouse model.Theranostics · 2025Article
- Serum proteomics reveal APOE-ε4-dependent and APOE-ε4-independent protein signatures in Alzheimer's disease.Nature aging · 2024Article
- Serum proteomics reveals APOE dependent and independent protein signatures in Alzheimer's disease.Research square · 2024Article
- Dem-Aging: autophagy-related pathologies and the "two faces of dementia".Neurogenetics · 2024Article
- Biomarkers in 5q-associated spinal muscular atrophy-a narrative review.Journal of neurology · 2023Review
- Reciprocal effects of alpha-synuclein aggregation and lysosomal homeostasis in synucleinopathy models.Translational neurodegeneration · 2023Article
- Alzheimer's Disease: An Updated Overview of Its Genetics.International journal of molecular sciences · 2023Review
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- A modified density gradient proteomic-based method to analyze endolysosomal proteins in cardiac tissue.iScience · 2021Article
- Tau Protein Interaction Partners and Their Roles in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2021Review
- Comparative analysis reveals distinctive epigenetic features of the human cerebellum.PLoS genetics · 2021Article
- Autophagy-targeted therapy to modulate age-related diseases: Success, pitfalls, and new directions.Current research in pharmacology and drug discovery · 2021Review
- Article
- An Overview of Astrocyte Responses in Genetically Induced Alzheimer's Disease Mouse Models.Cells · 2020Review
Corrections and comments
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Authors and funding
41 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although several ADAMs (A disintegrin-like and metalloproteases) have been shown to contribute to the amyloid precursor protein (APP) metabolism, the full spectrum of metalloproteases involved in this metabolism remains to be established. Transcriptomic analyses centred on metalloprotease genes unraveled a 50% decrease in ADAM30 expression that inversely correlates with amyloid load in Alzheimer's disease brains. Accordingly, in vitro down- or up-regulation of ADAM30 expression triggered an increase/decrease in Aβ peptides levels whereas expression of a biologically inactive ADAM30 (ADAM30(mut)) did not affect Aβ secretion. Proteomics/cell-based experiments showed that ADAM30-dependent regulation of APP metabolism required both cathepsin D (CTSD) activation and APP sorting to lysosomes. Accordingly, in Alzheimer-like transgenic mice, neuronal ADAM30 over-expression lowered Aβ42 secretion in neuron primary cultures, soluble Aβ42 and amyloid plaque load levels in the brain and concomitantly enhanced CTSD activity and finally rescued long term potentiation alterations. Our data thus indicate that lowering ADAM30 expression may favor Aβ production, thereby contributing to Alzheimer's disease development.
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Registered trials
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.