ReviewThe Lancet. Neurology2008
Amyloid-beta immunisation for Alzheimer's disease.
Review in The Lancet. Neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 156 citations in OpenAlex.
- Sodium benzoate treatment decreased amyloid beta peptides and improved cognitive function among patients with Alzheimer's disease: secondary analysis of a randomized clinical trial.Translational psychiatry · 2025Trial
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Unraveling the Complexity of Alzheimer's Disease: Insights into Etiology and Advancements in Treatment Strategies.Journal of molecular neuroscience : MN · 2025Review
- Second-generation anti-amyloid monoclonal antibodies for Alzheimer's disease: current landscape and future perspectives.Translational neurodegeneration · 2025Review
- Identification of Phytoconstituents from Natural Product Database as SIRT2 Inhibitors for Potential Role in Alzheimer's Disease: An In-Silico Screening.Central nervous system agents in medicinal chemistry · 2025Article
- Review
- Recent Advances in the Treatment and Management of Alzheimer's Disease: A Precision Medicine Perspective.Current topics in medicinal chemistry · 2024Review
- Alzheimer Disease: A Life-Limiting Disease With a Burden of a Terminal Illness.Neurology. Clinical practice · 2023Review
- Nucleic acid drug vectors for diagnosis and treatment of brain diseases.Signal transduction and targeted therapy · 2023Review
- Antibody-Mediated Clearance of Brain Amyloid-β: Mechanisms of Action, Effects of Natural and Monoclonal Anti-Aβ Antibodies, and Downstream Effects.Journal of Alzheimer's disease reports · 2023Review
- Focal-type, but not Diffuse-type, Amyloid Beta Plaques are Correlated with Alzheimer's Neuropathology, Cognitive Dysfunction, and Neuroinflammation in the Human Hippocampus.Neuroscience bulletin · 2022Article
- Adoptive therapy with amyloid-β specific regulatory T cells alleviates Alzheimer's disease.Theranostics · 2022Article
- Interaction between autophagy and the NLRP3 inflammasome in Alzheimer's and Parkinson's disease.Frontiers in aging neuroscience · 2022Review
- Targeting innate immunity to protect and cure Alzheimer's disease: opportunities and pitfalls.Molecular psychiatry · 2021Review
- Microfluidic Platforms to Unravel Mysteries of Alzheimer's Disease: How Far Have We Come?Life (Basel, Switzerland) · 2021Review
- Article
- Recent advances in tau-directed immunotherapy against Alzheimer's disease: an overview of pre-clinical and clinical development.Metabolic brain disease · 2020Review
- Tryptophan-galactosylamine conjugates inhibit and disaggregate amyloid fibrils of Aβ42 and hIAPP peptides while reducing their toxicity.Communications biology · 2020Article
- Small molecule probes of protein aggregation.Current opinion in chemical biology · 2017Review
- Evaluation of Novel Dual Acetyl- and Butyrylcholinesterase Inhibitors as Potential Anti-Alzheimer's Disease Agents Using Pharmacophore, 3D-QSAR, and Molecular Docking Approaches.Molecules (Basel, Switzerland) · 2017Article
20 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
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease is the main cause of dementia in elderly people and is becoming an ever greater problem as societies worldwide age. Treatments that stop or at least effectively modify disease course do not yet exist. In Alzheimer's disease, the conversion of the amyloid-beta peptide (Abeta) from a physiological water-soluble monomeric form into neurotoxic oligomeric and fibrillar forms rich in stable beta-sheet conformations is an important event. The most toxic forms of Abeta are thought to be oligomers, and dimers might be the smallest neurotoxic species. Numerous immunological approaches that prevent the conversion of the normal precursor protein into pathological forms or that accelerate clearance are in development. More than ten new approaches to active and passive immunotherapy are under investigation in clinical trials with the aim of producing safe methods for immunological therapy and prevention. A delicate balance between immunological clearance of an endogenous protein with acquired toxic properties and the induction of an autoimmune reaction must be found.
Indexed as
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.