ArticleCell reports2020
Identification of Conserved Proteomic Networks in Neurodegenerative Dementia.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 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
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.
- Pooled it
- Chromosome X-wide association study in case control studies of pathologically confirmed Alzheimer's disease in a European population.Translational psychiatry · 2024Pooled it
- Multi-omics technologies: Novel tools and methods for assessing nerve injury and regeneration.Neural regeneration research · 2026Article
- A critical appraisal of the link between apolipoprotein E and Tau.Current opinion in neurology · 2026Review
- Unravelling Synaptic and Metabolic Mechanisms of Cognitive Resilience in Asymptomatic Alzheimer's Disease Across Two Alzheimer's Disease Cohorts.Cellular and molecular neurobiology · 2026Article
- The evolution of Alzheimer's target identification: Towards a fusion of artificial and cellular intelligence.The journal of prevention of Alzheimer's disease · 2025Article
- Lysosomal proteomics reveals mechanisms of neuronal APOE4-associated lysosomal dysfunction.Autophagy · 2025Article
- Tau-seed interactome analysis reveals distinct functional signatures in Alzheimer's disease across model systems.bioRxiv : the preprint server for biology · 2025Article
- Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Lysosomal proteomics reveals mechanisms of neuronal apoE4-associated lysosomal dysfunction.bioRxiv : the preprint server for biology · 2025Article
- Spatial and single-nucleus transcriptomic analysis of genetic and sporadic forms of Alzheimer's disease.Nature genetics · 2024Article
- Brain-wide alterations revealed by spatial transcriptomics and proteomics in COVID-19 infection.Nature aging · 2024Article
- Cross-disorder and disease-specific pathways in dementia revealed by single-cell genomics.Cell · 2024Article
- Whole-genome sequencing analysis reveals new susceptibility loci and structural variants associated with progressive supranuclear palsy.Molecular neurodegeneration · 2024Article
- CSF Proteomics in Patients With Progressive Supranuclear Palsy.Neurology · 2024Article
- Network proteomics of the Lewy body dementia brain reveals presynaptic signatures distinct from Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Proteomic networks of gray and white matter reveal tissue-specific changes in human tauopathy.Annals of clinical and translational neurology · 2024Article
- Psychosocial experiences are associated with human brain mitochondrial biology.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- DLK-MAPK Signaling Coupled with DNA Damage Promotes Intrinsic Neurotoxicity Associated with Non-Mutated Tau.Molecular neurobiology · 2024Article
- Post-translational modifications linked to preclinical Alzheimer's disease-related pathological and cognitive changes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Data-driven analyses are increasingly valued in modern medicine. We integrate quantitative proteomics and transcriptomics from over 1,000 post-mortem brains from six cohorts representing Alzheimer's disease (AD), asymptomatic AD, progressive supranuclear palsy (PSP), and control patients from the Accelerating Medicines Partnership - Alzheimer's Disease consortium. We define robust co-expression trajectories related to disease progression, including early neuronal, microglial, astrocyte, and immune response modules, and later mRNA splicing and mitochondrial modules. The majority of, but not all, modules are conserved at the transcriptomic level, including module C3, which is only observed in proteome networks and enriched in mitogen-activated protein kinase (MAPK) signaling. Genetic risk enriches in modules changing early in disease and indicates that AD and PSP have distinct causal biological drivers at the pathway level, despite aspects of similar pathology, including synaptic loss and glial inflammatory changes. The conserved, high-confidence proteomic changes enriched in genetic risk represent targets for drug discovery.
Indexed as
Identifiers
What OpenQuestion holds
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.