ReviewAlzheimer's & dementia : the journal of the Alzheimer's Association2025
The case for regulatory approval of amyloid-lowering immunotherapies in Alzheimer's disease based on clearcut biomarker evidence.
Review in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Prognostic value of plasma %p-tau217 in cognitively unimpaired older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Amyloid-beta induces distinct forms of cell death in different neuronal populations.Cell death and differentiation · 2026Article
- Defining Alzheimer's disease: stipulations and the ethics of diagnostic change.Journal of neurology, neurosurgery, and psychiatry · 2026Article
- Modeling Alzheimer's disease through the integration of exposome, inflammasome, and connectome.Neural regeneration research · 2026Article
- Target product profiles for treatments to delay or prevent symptomatic Alzheimer's disease.Nature medicine · 2026Review
- A review of evidence supporting amyloid beta reduction as a surrogate endpoint in Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2026Review
- (±)-2-Cyclohexyl-5-methoxy-2H-chromene, a Synthetic 5-Methoxyflavone Derivative, Is a Selective DNA Polymerase-β Inhibitor with Neuroprotective Activity against β-Amyloid Toxicity.ACS chemical neuroscience · 2026Article
- Do Anti-Amyloid Antibodies Modulate Brain Function in Alzheimer's Disease?Neuro-degenerative diseases · 2026Article
- Towards pharmacological prevention of Alzheimer disease.Nature reviews. Neurology · 2025Review
- Amyloid quantification in the oldest-old: selecting regions for optimizing correspondence between postmortem pathology and amyloid PET.Acta neuropathologica communications · 2025Article
- CTAD taskforce: genetic therapies in Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Review
- Proteomic landscape of Alzheimer's disease: emerging technologies, advances and insights (2021 - 2025).Molecular neurodegeneration · 2025Review
- Amyloid immunotherapy for Alzheimer's disease: the case for cautious adoption.Arquivos de neuro-psiquiatria · 2025Review
- The science does not yet support regulatory approval of amyloid-targeting therapies for Alzheimer's disease based solely on biomarker evidence.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Maximizing the benefit and managing the risk of anti-amyloid monoclonal antibody therapy for Alzheimer's disease: Strategies and research directions.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Integrating genetic and immune profiles for personalized immunotherapy in Alzheimer's disease.Frontiers in medicine · 2025Review
- The case for regulatory approval of amyloid-lowering immunotherapies in Alzheimer's disease based on clearcut biomarker evidence.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Evaluation of amyloid change as a surrogate for cognitive decline: demonstration in individual-level data from the A4 study of solanezumab.Alzheimer's & dementia (New York, N. Y.)Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Decades of research have provided evidence that Alzheimer's disease (AD) is caused in part by cerebral accumulation of amyloid beta-protein (Aβ). In 2023, the US Food and Drug Administration gave full regulatory approval to a disease-modifying Aβ antibody for early AD. Secondary prevention trials with Aβ antibodies are underway. We summarize peer-reviewed evidence for targeting Aβ and argue that regulators should consider approving new agents working by similar mechanisms (Aβ antibodies and vaccines) based on robust amyloid lowering and reasonable safety. The urgent need to provide treatments to millions of mildly symptomatic patients suggests that AD should join other diseases for which standard approval is based on significant changes in mechanistically meaningful biomarkers coupled with safety. Robust amyloid lowering in secondary prevention trials of people who have amyloid plaques but are asymptomatic could also provide evidence of a change in the pathophysiological progression of AD as a basis for regulatory approval. HIGHLIGHTS: Thirteen key findings support amyloid beta as a cause of Alzheimer's disease (AD). Three immunotherapies lower amyloid and slow decline, allowing regulatory approval. New such agents could be considered for approval due to amyloid lowering and safety. Urgency suggests AD may join diseases with approval due to a key biomarker + safety.
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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.