ArticlePloS one2012
Amyloid-beta (Aβ) D7H mutation increases oligomeric Aβ42 and alters properties of Aβ-zinc/copper assemblies.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 119 citations in OpenAlex.
- Effect of the Tottori familial disease mutation (D7N) on the monomers and dimers of Aβ40 and Aβ42.ACS chemical neuroscience · 2013Trial
- K16F/E22F Mutation Promotes Oligomerization and Alters β-Sheet Topology of Aβ16-22 Peptides: Insights from Molecular Dynamics Simulations.ACS chemical neuroscience · 2026Article
- Aggregation-Dependent Epitope Sequence and Modification Fingerprints of Anti-Aβ Antibodies.bioRxiv : the preprint server for biology · 2025Article
- The Role of Neprilysin and Insulin-Degrading Enzyme in the Etiology of Sporadic Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Neuron-Astrocyte Interactions in Aging and Alzheimer's Disease: Dysregulation of Amyloid Precursor Protein.Ageing & longevity · 2025Article
- Transient interactions between the fuzzy coat and the cross-β core of brain-derived Aβ42 filaments.Science advances · 2025Article
- Review
- A turn for the worse: Aβ β-hairpins in Alzheimer's disease.Bioorganic & medicinal chemistry · 2024Review
- E674Q (ShanghaiGenes & diseases · 2024Article
- Article
- Death-associated protein kinase 1 as a therapeutic target for Alzheimer's disease.Translational neurodegeneration · 2024Review
- Molecular Mechanism of Zinc-Dependent Oligomerization of Alzheimer's Amyloid-β with Taiwan (D7H) Mutation.International journal of molecular sciences · 2023Article
- Neuroinflammation represents a common theme amongst genetic and environmental risk factors for Alzheimer and Parkinson diseases.Journal of neuroinflammation · 2022Review
- Clinical characteristics and genotype-phenotype correlation analysis of familial Alzheimer's disease patients with pathogenic/likely pathogenic amyloid protein precursor mutations.Frontiers in aging neuroscience · 2022Article
- Degradation of FA reduces Aβ neurotoxicity and Alzheimer-related phenotypes.Molecular psychiatry · 2021Article
- Article
- Gene mutations associated with early onset familial Alzheimer's disease in China: An overview and current status.Molecular genetics & genomic medicine · 2020Review
- The English (H6R) Mutation of the Alzheimer's Disease Amyloid-β Peptide Modulates Its Zinc-Induced Aggregation.Biomolecules · 2020Article
- Central and Peripheral Metabolic Defects Contribute to the Pathogenesis of Alzheimer's Disease: Targeting Mitochondria for Diagnosis and Prevention.Antioxidants & redox signaling · 2020Review
- The Genetics of Alzheimer's Disease in the Chinese Population.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation. Here, we identified a novel APP mutation, located within the Aβ sequence (Aβ(D7H)), in a Taiwanese family with early onset AD and explored the pathogenicity of this mutation. Cellular and biochemical analysis reveal that this mutation increased Aβ production, Aβ42/40 ratio and prolonged Aβ42 oligomer state with higher neurotoxicity. Because the D7H mutant Aβ has an additional metal ion-coordinating residue, histidine, we speculate that this mutation may promote susceptibility of Aβ to ion. When co-incubated with Zn(2+) or Cu(2+), Aβ(D7H) aggregated into low molecular weight oligomers. Together, the D7H mutation could contribute to AD pathology through a "double punch" effect on elevating both Aβ production and oligomerization. Although the pathogenic nature of this mutation needs further confirmation, our findings suggest that the Aβ N-terminal region potentially modulates APP processing and Aβ aggregation, and further provides a genetic indication of the importance of Zn(2+) and Cu(2+) in the etiology of AD.
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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.