ArticleProceedings of the National Academy of Sciences of the United States of America2022
SOBA: Development and testing of a soluble oligomer binding assay for detection of amyloidogenic toxic oligomers.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 66 citations in OpenAlex.
- Pathogenic landscape shaped by cerebral amyloid oligomers.Neural regeneration research · 2026Article
- Localized amyloid-β oligomers in the lateral entorhinal cortex drives olfactory dysfunction through aberrant neuronal and network activity.Acta neuropathologica communications · 2026Article
- Endogenously generated Dutch-type Aβ non-fibrillar aggregates dysregulate presynaptic neurotransmission in the absence of detectable inflammation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Characterization of conformation-specific antibodies TOMA-1 and TTCM-1 for recombinant tau monomer and amplified brain derived tau oligomer.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Clinical and Cognitive Profiles of Individuals with Alzheimer's Disease and Comorbid Seizures.Annals of neurology · 2025Article
- Circulating Biomarkers for the Early Diagnosis of Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Immunization targeting diseased proteins in synucleinopathy and tauopathy: insights from clinical trials.Translational neurodegeneration · 2025Review
- Blood-based quantification of Aβ oligomers indicates impaired clearance from brain in ApoE ε4 positive subjects.Communications medicine · 2024Article
- Alzheimer's Disease: Exploring the Landscape of Cognitive Decline.ACS chemical neuroscience · 2024Review
- Molecular properties and diagnostic potential of monoclonal antibodies targeting cytotoxic α-synuclein oligomers.NPJ Parkinson's disease · 2024Article
- Designed De Novo α-Sheet Peptides Destabilize Bacterial Biofilms and Increase the Susceptibility ofInternational journal of molecular sciences · 2024Article
- Progress on early diagnosing Alzheimer's disease.Frontiers of medicine · 2024Review
- Considerations for biomarker strategies in clinical trials investigating tau-targeting therapeutics for Alzheimer's disease.Translational neurodegeneration · 2024Review
- Plasma biomarkers for Alzheimer's and related dementias: A review and outlook for clinical neuropsychology.Archives of clinical neuropsychology : the official journal of the National Academy of Neuropsychologists · 2024Review
- Performance of SOBA-AD blood test in discriminating Alzheimer's disease patients from cognitively unimpaired controls in two independent cohorts.Scientific reports · 2024Article
- Article
- Lewy body dementia: Overcoming barriers and identifying solutions.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Human islet amyloid polypeptide-induced β-cell cytotoxicity is linked to formation of α-sheet structure.Protein science : a publication of the Protein Society · 2024Article
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The formation of toxic Amyloid β-peptide (Aβ) oligomers is one of the earliest events in the molecular pathology of Alzheimer's Disease (AD). These oligomers lead to a variety of downstream effects, including impaired neuronal signaling, neuroinflammation, tau phosphorylation, and neurodegeneration, and it is estimated that these events begin 10 to 20 y before the presentation of symptoms. Toxic Aβ oligomers contain a nonstandard protein structure, termed α-sheet, and designed α-sheet peptides target this main-chain structure in toxic oligomers independent of sequence. Here we show that a designed α-sheet peptide inhibits the deleterious effects on neuronal signaling and also serves as a capture agent in our soluble oligomer binding assay (SOBA). Pre-incubated synthetic α-sheet-containing Aβ oligomers produce strong SOBA signals, while monomeric and β-sheet protofibrillar Aβ do not. α-sheet containing oligomers were also present in cerebrospinal fluid (CSF) from an AD patient versus a noncognitively impaired control. For the detection of toxic oligomers in plasma, we developed a plate coating to increase the density of the capture peptide. The proof of concept was achieved by testing 379 banked human plasma samples. SOBA detected Aβ oligomers in patients on the AD continuum, including controls who later progressed to mild cognitive impairment. In addition, SOBA discriminated AD from other forms of dementia, yielding sensitivity and specificity of 99% relative to clinical and neuropathological diagnoses. To explore the broader potential of SOBA, we adapted the assay for a-synuclein oligomers and confirmed their presence in CSF from patients with Parkinson's disease and Lewy body dementia.
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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.