ReviewInternational journal of molecular sciences2021
Neurotoxic Soluble Amyloid Oligomers Drive Alzheimer's Pathogenesis and Represent a Clinically Validated Target for Slowing Disease Progression.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 210 citations in OpenAlex.
- Ultrasound-induced blood-brain barrier opening in Alzheimer's disease: a systematic review of clinical studies.Aging clinical and experimental research · 2026Pooled it
- Efficacy of the visual cognitive assessment test for mild cognitive impairment/mild dementia diagnosis: a meta-analysis.Frontiers in public health · 2023Pooled it
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- Trial
- Biofluid biomarker changes following treatment with sabirnetug (ACU193) in INTERCEPT-AD, a phase 1 trial in early Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Trial
- Clinical Pharmacokinetics of Oral ALZ-801/Valiltramiprosate in a 2-Year Phase 2 Trial of APOE4 Carriers with Early Alzheimer's Disease.Clinical pharmacokinetics · 2025Trial
- Trial
- Trial
- Evaluation of tau deposition usingAlzheimer's research & therapy · 2022Trial
- TPPU, a soluble epoxide hydrolase inhibitor, mitigates Aβ-induced neurotoxicity via dual modulation of mitochondrial stabilization and JNK suppression.Biochemistry and biophysics reports · 2026Article
- Article
- Blood-based biomarkers and early diagnosis of Alzheimer's disease.Neural regeneration research · 2026Article
- Aggregation of Amyloid-like Peptides in Different Solvents.Journal of molecular liquids · 2026Article
- When copper turns killer: Decoding copper dyshomeostasis and cuproptosis in neurodegenerative pathogenesis and precision metal interventions.Neural regeneration research · 2026Article
- Article
- The Effect of CuACS chemical neuroscience · 2026Article
- Investigating a relation between amyloid beta plaque burden and accumulated neurotoxicity caused by amyloid beta oligomers.Medical & biological engineering & computing · 2026Article
- Advances in nano-TCM for Alzheimer's disease: lipid-based carriers integrated with innovative delivery strategies.Journal of nanobiotechnology · 2026Review
- Ischemic injury triggers a protective microglial phenotype in models of Aβ pathology.Journal of neuroinflammation · 2026Article
- Multitarget Actions of Pentacyclic Triterpenic Acids in Alzheimer's Disease: Mechanistic Insights.Molecules (Basel, Switzerland) · 2026Review
73 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large body of clinical and nonclinical evidence supports the role of neurotoxic soluble beta amyloid (amyloid, Aβ) oligomers as upstream pathogenic drivers of Alzheimer's disease (AD). Recent late-stage trials in AD that have evaluated agents targeting distinct species of Aβ provide compelling evidence that inhibition of Aβ oligomer toxicity represents an effective approach to slow or stop disease progression: (1) only agents that target soluble Aβ oligomers show clinical efficacy in AD patients; (2) clearance of amyloid plaque does not correlate with clinical improvements; (3) agents that predominantly target amyloid monomers or plaque failed to show clinical effects; and (4) in positive trials, efficacy is greater in carriers of the ε4 allele of apolipoprotein E (APOE4), who are known to have higher brain concentrations of Aβ oligomers. These trials also show that inhibiting Aβ neurotoxicity leads to a reduction in tau pathology, suggesting a pathogenic sequence of events where amyloid toxicity drives an increase in tau formation and deposition. The late-stage agents with positive clinical or biomarker data include four antibodies that engage Aβ oligomers (aducanumab, lecanemab, gantenerumab, and donanemab) and ALZ-801, an oral agent that fully blocks the formation of Aβ oligomers at the clinical dose.
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Identifiers
What OpenQuestion holds
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.