ArticleActa neuropathologica2017
Proteomic differences in amyloid plaques in rapidly progressive and sporadic Alzheimer's disease.
Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 4 of them syntheses that pooled it.
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
133 citing papers in PubMed, 4 syntheses or guidelines pooled it, 243 citations in OpenAlex.
- Pooled it
- Shift of the insoluble content of the proteome in the aging mouse brain.Proceedings of the National Academy of Sciences of the United States of America · 2023Pooled it
- Dissecting Detergent-Insoluble Proteome in Alzheimer's Disease by TMTc-Corrected Quantitative Mass Spectrometry.Molecular & cellular proteomics : MCP · 2023Pooled it
- Insights into the changes in the proteome of Alzheimer disease elucidated by a meta-analysis.Scientific data · 2021Pooled it
- Atypical Alzheimer disease: a multi-axis framework toward defining heterogeneity.Nature reviews. Neurology · 2026Review
- Apolipoprotein D acts as a chaperone of Aβ peptide delaying its assembly into amyloid aggregates.Cellular and molecular life sciences : CMLS · 2026Article
- Early, sex-dependent and progressive proteomic imbalance in the amygdala during Alzheimer´s disease continuum.Biology of sex differences · 2026Article
- Article
- Evidence for different seeding activities of misfolded tau in classical and rapidly progressive Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- The Amyloid Plaque Proteomes of Alzheimer's Disease and Mild Cognitive Impairment.Research square · 2026Article
- Prevalence and clinical effects of Lewy Body pathology in non-prion rapidly progressive dementias: a retrospective cohort study.Alzheimer's research & therapy · 2026Article
- Single Plaque Proteomics Reveals the Composition and Dynamics of the Amyloid Microenvironment in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Proteome-Based Biomarkers for Alzheimer's Disease: Old Acquisitions and Innovative Proposals.International journal of molecular sciences · 2025Review
- Aβ Modulates Extracellular Vesicles Proteomic Profile Impacting Phosphorylation Mediators.Molecular neurobiology · 2025Article
- Association of Platelet Aggregation With Markers of Alzheimer Disease Pathology in Middle-Aged Participants of the Framingham Heart Study.Neurology · 2025Article
- Proteomic Profiling Reveals Mitochondrial Dysregulation in Rapidly Progressive Alzheimer's: Role of DLDH in Amyloid Beta Aggregation.Molecular neurobiology · 2025Article
- Region-specific proteomic analysis of aging rhesus macaques following chronic glutamate-carboxypeptidase-II (GCPII) inhibition elucidates potential treatment strategies for sporadic Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Species-specific sensitivity to intracerebroventricular streptozotocin in rats and mice highlights pathways and proteins relevant to Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Overview of Proteomic Analysis of Amyloid Plaques and Neurofibrillary Tangles in Alzheimer's Disease.Biomolecules · 2025Review
- Profiling RNA Cargo in Extracellular Vesicles From hiPSC-Derived Neurons of Alzheimer's Disease Patients.Journal of extracellular biology · 2025Article
73 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
14 authors at 3 institutions in 1 country.
Funding
Abstract
Rapidly progressive Alzheimer's disease (rpAD) is a particularly aggressive form of Alzheimer's disease, with a median survival time of 7-10 months after diagnosis. Why these patients have such a rapid progression of Alzheimer's disease is currently unknown. To further understand pathological differences between rpAD and typical sporadic Alzheimer's disease (sAD) we used localized proteomics to analyze the protein differences in amyloid plaques in rpAD and sAD. Label-free quantitative LC-MS/MS was performed on amyloid plaques microdissected from rpAD and sAD patients (n = 22 for each patient group) and protein expression differences were quantified. On average, 913 ± 30 (mean ± SEM) proteins were quantified in plaques from each patient and 279 of these proteins were consistently found in plaques from every patient. We found significant differences in protein composition between rpAD and sAD plaques. We found that rpAD plaques contained significantly higher levels of neuronal proteins (p = 0.0017) and significantly lower levels of astrocytic proteins (p = 1.08 × 10
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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.