ReviewNature reviews. Neurology2010
Can Alzheimer disease be prevented by amyloid-beta immunotherapy?
Review in Nature reviews. Neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 174 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
174 citing papers in PubMed, 346 citations in OpenAlex.
- Ferro-aging: a potential driver of degenerative bone and joint diseases.Cell communication and signaling : CCS · 2026Review
- Neurodegenerative diseases and immune system: From pathogenic mechanism to therapy.Neural regeneration research · 2026Article
- ACSL4 in Alzheimer's disease: Pathogenetic mechanisms and potential therapeutic targets.Genes & diseases · 2026Review
- Early binding of anti-amyloid antibodies to CAA drives complement activation, inflammation and ARIA in mice.Molecular neurodegeneration · 2026Article
- α/Sulfonyl-γ-AApeptide foldamers mitigate Alzheimer's disease pathology by stabilizing transient helical domains in Aβ.Nature communications · 2026Article
- Advancements in Gene Delivery using Nucleic Acid Loaded Nanoparticles for Region Specific Delivery in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Early Binding of Anti-Amyloid Antibodies to CAA Drives Complement Activation, Inflammation and ARIA in Mice.bioRxiv : the preprint server for biology · 2026Article
- Microglial low-affinity FcγR mediates the phagocytic elimination of dopaminergic neurons in Parkinson's disease degeneration.NPJ Parkinson's disease · 2026Article
- Biologics as Therapeutical Agents Under Perspective Clinical Studies for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- An Overview of Glutaminyl Cyclase as a Promising Drug Target for Alzheimer's Disease.Biomedicines · 2025Article
- Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.Aging and disease · 2025Review
- Tripeptides inhibit dual targets AChE and BACE-1: a computational study.RSC advances · 2025Article
- Review
- Stem Cells as a Novel Source for Regenerative Medicinal Applications in Alzheimer's Disease: An Update.Current molecular medicine · 2025Review
- T cell independent antibody responses with class switch and memory using peptides anchored on liposomes.NPJ vaccines · 2024Article
- GluN2B subunit selective N-methyl-D-aspartate receptor ligands: Democratizing recent progress to assist the development of novel neurotherapeutics.Molecular diversity · 2024Review
- Anti-Amyloid Immunotherapies for Alzheimer's Disease: A 2023 Clinical Update.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Amyloid β-based therapy for Alzheimer's disease: challenges, successes and future.Signal transduction and targeted therapy · 2023Review
- Recent Trends in Active and Passive Immunotherapies of Alzheimer's Disease.Antibodies (Basel, Switzerland) · 2023Review
- Alzheimer's Disease: A Brief History of Immunotherapies Targeting Amyloid β.International journal of molecular sciences · 2023Review
114 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer disease (AD) is the most common form of dementia. The amyloid-beta (Abeta) peptide has become a major therapeutic target in AD on the basis of pathological, biochemical and genetic evidence that supports a role for this molecule in the disease process. Active and passive Abeta immunotherapies have been shown to lower cerebral Abeta levels and improve cognition in animal models of AD. In humans, dosing in the phase II clinical trial of the AN1792 Abeta vaccine was stopped when approximately 6% of the immunized patients developed meningoencephalitis. However, some plaque clearance and modest clinical improvements were observed in patients following immunization. As a result of this study, at least seven passive Abeta immunotherapies are now in clinical trials in patients with mild to moderate AD. Several second-generation active Abeta vaccines are also in early clinical trials. On the basis of preclinical studies and the limited data from clinical trials, Abeta immunotherapy might be most effective in preventing or slowing the progression of AD when patients are immunized before or in the very earliest stages of disease onset. Biomarkers for AD and imaging technology have improved greatly over the past 10 years and, in the future, might be used to identify presymptomatic, at-risk individuals who might benefit from Abeta immunization.
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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.