ArticleProteomics2016
Changes in the detergent-insoluble brain proteome linked to amyloid and tau in Alzheimer's Disease progression.
Article in Proteomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- 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
- Meta-Analysis of Gene Expression Changes in the Blood of Patients with Mild Cognitive Impairment and Alzheimer's Disease Dementia.International journal of molecular sciences · 2019Pooled it
- Neuroproteasomes regulate endogenous tau paired helical filament formation in an APOE genotype- and age-dependent manner.Nature neuroscience · 2026Article
- Aβ Aggregates Bind the U1 Spliceosomal Ribonucleoprotein in Alzheimer Disease Brain.bioRxiv : the preprint server for biology · 2026Article
- Shifts in protein aggregate stability define proteostasis decline in the aging human brain.bioRxiv : the preprint server for biology · 2026Article
- A distinct tau oligomer strain defines the molecular and proteomic landscape of rapidly progressive Alzheimer's disease.Acta neuropathologica · 2026Article
- Single Plaque Proteomics Reveals the Composition and Dynamics of the Amyloid Microenvironment in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Neuronal subtype governs amyloid structure, cellular response, and cognitive outcome in genetically targeted APP mouse models.Molecular neurodegeneration · 2026Article
- 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
- Integrative brain omics approach highlights sn-1 lysophosphatidylethanolamine in Alzheimer's dementia.Nature communications · 2025Article
- HAPLN2 forms aggregates and promotes microglial inflammation during brain aging in mice.PLoS biology · 2025Article
- A Novel Spectral Barcoding and Classification Approach for Complex Biological Samples Using Multiexcitation Raman Spectroscopy (MX-Raman).Analytical chemistry · 2025Article
- Analysis of the splicing landscape of the frontal cortex in FTLD-TDP reveals subtype specific patterns and cryptic splicing.Acta neuropathologica · 2025Article
- Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025Article
- Effects of the therapeutic correction of U1 snRNP complex on Alzheimer's disease.Scientific reports · 2024Article
- Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation.PLoS genetics · 2024Article
- Article
- Proteomic networks of gray and white matter reveal tissue-specific changes in human tauopathy.Annals of clinical and translational neurology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Despite a key role of amyloid-beta (Aβ) in Alzheimer's disease (AD), mechanisms that link Aβ plaques to tau neurofibrillary tangles and cognitive decline still remain poorly understood. The purpose of this study was to quantify proteins in the sarkosyl-insoluble brain proteome correlated with Aβ and tau insolubility in the asymptomatic phase of AD (AsymAD) and through mild cognitive impairment (MCI) and symptomatic AD. Employing label-free mass spectrometry-based proteomics, we quantified 2711 sarkosyl-insoluble proteins across the prefrontal cortex from 35 individual cases representing control, AsymAD, MCI and AD. Significant enrichment of Aβ and tau in AD was observed, which correlated with neuropathological measurements of plaque and tau tangle density, respectively. Pairwise correlation coefficients were also determined for all quantified proteins to Aβ and tau, across the 35 cases. Notably, six of the ten most correlated proteins to Aβ were U1 small nuclear ribonucleoproteins (U1 snRNPs). Three of these U1 snRNPs (U1A, SmD and U1-70K) also correlated with tau consistent with their association with tangle pathology in AD. Thus, proteins that cross-correlate with both Aβ and tau, including specific U1 snRNPs, may have potential mechanistic roles in linking Aβ plaques to tau tangle pathology during AD progression.
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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.