ArticleNature neuroscience2020
Acute targeting of pre-amyloid seeds in transgenic mice reduces Alzheimer-like pathology later in life.
Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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.
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Who cites it
47 citing papers in PubMed, 81 citations in OpenAlex.
- Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.Brain communications · 2026Article
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
- Acute targeting of N-terminal tau protein has long-lasting beneficial effects in Tg2576 APP/Aβ mouse model by reducing cognitive impairment, cerebral Aβ-amyloidosis, synaptic remodeling and microgliosis later in life.Acta neuropathologica communications · 2025Article
- Experimental evidence that readily diffusible forms of Aβ from Alzheimer's disease brain have seeding activity.Acta neuropathologica communications · 2025Article
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Sleep deprivation leads to non-adaptive alterations in sleep microarchitecture and amyloid-β accumulation in a murine Alzheimer model.Cell reports · 2024Article
- The prion principle and Alzheimer's disease.Science (New York, N.Y.) · 2024Article
- Exploring microtubule dynamics in Alzheimer's disease: Longitudinal assessment using [Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- The Single Toxin Origin of Alzheimer's Disease and Other Neurodegenerative Disorders Enables Targeted Approach to Treatment and Prevention.International journal of molecular sciences · 2024Review
- Amyloid-β in Alzheimer's disease: Structure, toxicity, distribution, treatment, and prospects.Ibrain · 2024Review
- Review
- βNature neuroscience · 2023Article
- Long-term effects of immunotherapy with a brain penetrating Aβ antibody in a mouse model of Alzheimer's disease.Alzheimer's research & therapy · 2023Article
- Alzheimer's Disease: A Brief History of Immunotherapies Targeting Amyloid β.International journal of molecular sciences · 2023Review
- A novel human tau knock-in mouse model reveals interaction of Abeta and human tau under progressing cerebral amyloidosis in 5xFAD mice.Alzheimer's research & therapy · 2023Article
- Shifting the balance: soluble ADAM10 as a potential treatment for Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Misfolded amyloid-β strains and their potential roles in the clinical and pathological variability of Alzheimer's disease.Neural regeneration research · 2023Article
- A glance through the effects of CD4Computational and structural biotechnology journal · 2023Review
- Amyloid oligomers as on-pathway precursors or off-pathway competitors of fibrils.Frontiers in molecular biosciences · 2023Review
- Article
Corrections and comments
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Authors and funding
26 authors at 6 institutions in 3 countries.
Funding
Abstract
Amyloid-β (Aβ) deposits are a relatively late consequence of Aβ aggregation in Alzheimer's disease. When pathogenic Aβ seeds begin to form, propagate and spread is not known, nor are they biochemically defined. We tested various antibodies for their ability to neutralize Aβ seeds before Aβ deposition becomes detectable in Aβ precursor protein-transgenic mice. We also characterized the different antibody recognition profiles using immunoprecipitation of size-fractionated, native, mouse and human brain-derived Aβ assemblies. At least one antibody, aducanumab, after acute administration at the pre-amyloid stage, led to a significant reduction of Aβ deposition and downstream pathologies 6 months later. This demonstrates that therapeutically targetable pathogenic Aβ seeds already exist during the lag phase of protein aggregation in the brain. Thus, the preclinical phase of Alzheimer's disease-currently defined as Aβ deposition without clinical symptoms-may be a relatively late manifestation of a much earlier pathogenic seed formation and propagation that currently escapes detection in vivo.
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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.