ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2015
β-Amyloid peptides and amyloid plaques in Alzheimer's disease.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 4 of them syntheses that pooled it.
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
157 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- Plasma Biomarkers for Alzheimer's Disease Across the Continuum: A Systematic Review of SIMOA-Based Studies.Cellular and molecular neurobiology · 2026Pooled it
- Pooled it
- Salivary Biomarkers for Alzheimer's Disease: A Systematic Review with Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Neurogranin as a cognitive biomarker in cerebrospinal fluid and blood exosomes for Alzheimer's disease and mild cognitive impairment.Translational psychiatry · 2020Pooled it
- Aβ-42 Side Chain Deamidation at Q15 or N27 Modulates Protein Aggregation and Alters Microglial Cytokines and CD68.ACS chemical neuroscience · 2026Article
- Magnetic induction heating: where will the field go next?Chemical Society reviews · 2026Review
- Amyloid-β plaque diversity across brain regions in Alzheimer's disease and its relation to major clinicopathological traits.Acta neuropathologica · 2026Article
- Spontaneous aging of mature amyloids alters structural stability, cytotoxicity, and susceptibility to biological clearance.Cell death discovery · 2026Article
- Vitamin D Signaling in Neurodegenerative Disorders: Mechanisms, Therapeutic Potential, and Clinical Implications.Nutrients · 2026Review
- [Bushen Yijing Formula attenuates amyloid β-protein deposi-tion and oxidative damage inZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- The effects of polysaccharides fromHistology and histopathology · 2026Article
- Bridging pathologies: Mechanistic insights into the diabetes-Alzheimer's nexus.EXCLI journal · 2026Review
- Article
- Molecular mechanisms underlying p62-dependent secretion of the Alzheimer-associated ubiquitin variant UBBProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Region-Specific Expression Patterns of lncRNAs in the Central Nervous System: Cross-Species Comparison and Functional Insights.International journal of molecular sciences · 2025Article
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Pathological findings from surgical specimens and long-term outcome in cerebral amyloid angiopathy patients with intracerebral hemorrhage.Scientific reports · 2025Article
- Crocin Ameliorates Cognitive Impairment and Pathological Changes in Alzheimer's Disease Model Mice by Regulating Gut Microbiota.Food science & nutrition · 2025Article
- In Vitro Evaluation of Amide-Linked Coumarin Scaffolds for the Inhibition of α‑Synuclein and Tau Aggregation.ACS omega · 2025Article
97 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many lines of evidence support that β-amyloid (Aβ) peptides play an important role in Alzheimer's disease (AD), the most common cause of dementia. But despite much effort the molecular mechanisms of how Aβ contributes to AD remain unclear. While Aβ is generated from its precursor protein throughout life, the peptide is best known as the main component of amyloid plaques, the neuropathological hallmark of AD. Reduction in Aβ has been the major target of recent experimental therapies against AD. Unfortunately, human clinical trials targeting Aβ have not shown the hoped-for benefits. Thus, doubts have been growing about the role of Aβ as a therapeutic target. Here we review evidence supporting the involvement of Aβ in AD, highlight the importance of differentiating between various forms of Aβ, and suggest that a better understanding of Aβ's precise pathophysiological role in the disease is important for correctly targeting it for potential future therapy.
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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.