ArticleProceedings of the National Academy of Sciences of the United States of America2023
A possible mechanism for the enhanced toxicity of beta-amyloid protofibrils in Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- Use of high-affinity scFv antibody NUsc1 for isolation and sensitive detection of Alzheimer's-associated amyloid beta oligomers.The Journal of biological chemistry · 2026Article
- Immunomagnetic reduction detects amyloid β 1-42, but neitherRSC advances · 2026Article
- Passive amyloid-β immunotherapy in Alzheimer's disease: a multicellular clearance system beyond plaque removal.Molecular neurodegeneration · 2026Review
- The Double-Edged Sword Effect of the Fibrinolytic System in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Thermodynamic stability modulates chaperone-mediated disaggregation of α-synuclein fibrils.Chemical science · 2026Article
- Aging modulates amyloid clearance kinetics during anti-amyloid therapy: evidence from real-world serial amyloid PET.Frontiers in aging neuroscience · 2026Article
- Biflavonoids can Potentially Inhibit Amyloid Beta Internalization to Mitigate Its Cytotoxic Events.Molecular nutrition & food research · 2026Article
- Amyloid-Related Imaging Abnormality (ARIA) Beyond the APOE-ε4 Allele.Chronic diseases and translational medicine · 2025Review
- Formation of a β-Endorphin Corona Mitigates Alzheimer's Amyloidogenesis.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Antiamyloid Therapy and Cerebral Blood Flow Changes on MRI: A Potential Longitudinal Biomarker of Treatment Response?AJNR. American journal of neuroradiology · 2025Article
- N-Alkylamino Stilbene Compounds as Amyloid β Inhibitors for Alzheimer's Disease Research.Molecules (Basel, Switzerland) · 2025Article
- PF-06447475 Molecule Attenuates the Neuropathology of Familial Alzheimer's and Coexistent Parkinson's Disease Markers in PSEN1 I416T Dopaminergic-like Neurons.Molecules (Basel, Switzerland) · 2025Article
- Aquaporin 4 modulation drives amyloid burden and cognitive abilities in an APPPS1 mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A subcellular sampling instrument allows spatial resolution of amyloid deposit-derived organelle-specific effects in microglia.Communications biology · 2025Article
- Cognitive impairment in Sjogren's syndrome: Interplay between BACE1 activity, inflammatory blood biomarkers and neurocognitive testing.PloS one · 2025Article
- Mapping cellular stress and lipid dysregulation in Alzheimer-related progressive neurodegeneration using label-free Raman microscopy.Communications biology · 2024Article
- Alzheimer's Disease: Combination Therapies and Clinical Trials for Combination Therapy Development.CNS drugs · 2024Review
- Lutein from Chicken Eggs Prevents Amyloid β-Peptide Aggregation In Vitro and Amyloid β-Induced Inflammation in Human Macrophages (THP-1).ACS omega · 2024Article
- Lecanemab blocks the effects of the Aβ/fibrinogen complex on blood clots and synapse toxicity in organotypic culture.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Contactless edema via plasmin.Blood · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The amyloid-beta peptide (Aβ) is a driver of Alzheimer's disease (AD). Aβ monomers can aggregate and form larger soluble (oligomers/protofibrils) and insoluble (fibrils) forms. There is evidence that Aβ protofibrils are the most toxic form, but the reasons are not known. Consistent with a critical role for this form of Aβ in AD, a recently FDA-approved therapeutic antibody targeted against protofibrils, lecanemab, slows the progression of AD in patients. The plasma contact system, which can promote coagulation and inflammation, has been implicated in AD pathogenesis. This system is activated by Aβ which could lead to vascular and inflammatory pathologies associated with AD. We show here that the contact system is preferentially activated by protofibrils of Aβ. Aβ protofibrils bind to coagulation factor XII and high molecular weight kininogen and accelerate the activation of the system. Furthermore, lecanemab blocks Aβ protofibril activation of the contact system. This work provides a possible mechanism for Aβ protofibril toxicity in AD and why lecanemab is therapeutically effective.
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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.