ArticleThe Biochemical journal2013
Differential contribution of isoaspartate post-translational modifications to the fibrillization and toxic properties of amyloid β and the Asn23 Iowa mutation.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- Post-Translational Modifications Distinguish Amyloid-β Isoforms in Cerebral Amyloid Angiopathy and Alzheimer's Disease.Journal of neurochemistry · 2025Article
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
- Stability of Protein Pharmaceuticals: Recent Advances.Pharmaceutical research · 2024Review
- FDA-approved carbonic anhydrase inhibitors reduce amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Hypertension and hyperhomocysteinemia as modifiable risk factors for Alzheimer's disease and dementia: New evidence, potential therapeutic strategies, and biomarkers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Article
- Article
- Alzheimer's amyloid β heterogeneous species differentially affect brain endothelial cell viability, blood-brain barrier integrity, and angiogenesis.Aging cell · 2020Article
- Do Post-Translational Modifications Influence Protein Aggregation in Neurodegenerative Diseases: A Systematic Review.Brain sciences · 2020Review
- Nrf2 activation through the PI3K/GSK-3 axis protects neuronal cells from Aβ-mediated oxidative and metabolic damage.Alzheimer's research & therapy · 2020Article
- Impact of Tau on Neurovascular Pathology in Alzheimer's Disease.Frontiers in neurology · 2020Review
- A New Kid on the Block? Carbonic Anhydrases as Possible New Targets in Alzheimer's Disease.International journal of molecular sciences · 2019Review
- Structure of amyloid-β (20-34) with Alzheimer's-associated isomerization at Asp23 reveals a distinct protofilament interface.Nature communications · 2019Article
- Endothelial Mitochondrial Dysfunction in Cerebral Amyloid Angiopathy and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Implications of Metal Binding and Asparagine Deamidation for Amyloid Formation.International journal of molecular sciences · 2018Review
- Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity.Aging cell · 2018Article
- Traumatic Brain Injury and Alzheimer's Disease: The Cerebrovascular Link.EBioMedicine · 2018Review
- Pyroglutamate and Isoaspartate modified Amyloid-Beta in ageing and Alzheimer's disease.Acta neuropathologica communications · 2018Article
- Aβ truncated species: Implications for brain clearance mechanisms and amyloid plaque deposition.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mutations within the Aβ (amyloid β) peptide, especially those clustered at residues 21-23, are linked to early-onset AD (Alzheimer's disease) and primarily associated with cerebral amyloid angiopathy. The Iowa variant, a substitution of an aspartic acid residue for asparagine at position 23 (D23N), associates with widespread vascular amyloid and abundant diffuse pre-amyloid lesions significantly exceeding the incidence of mature plaques. Brain Iowa deposits consist primarily of a mixture of mutated and non-mutated Aβ species exhibiting partial aspartate isomerization at positions 1, 7 and 23. The present study analysed the contribution of the post-translational modification and the D23N mutation to the aggregation/fibrillization and cell toxicity properties of Aβ providing insight into the elicited cell death mechanisms. The induction of apoptosis by the different Aβ species correlated with their oligomerization/fibrillization propensity and β-sheet content. Although cell toxicity was primarily driven by the D23N mutation, all Aβ isoforms tested were capable, albeit at different time frames, of eliciting comparable apoptotic pathways with mitochondrial engagement and cytochrome c release to the cytoplasm in both neuronal and microvascular endothelial cells. Methazolamide, a cytochrome c release inhibitor, exerted a protective effect in both cell types, suggesting that pharmacological targeting of mitochondria may constitute a viable therapeutic avenue.
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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.