ReviewMolecular brain2016
Insight of brain degenerative protein modifications in the pathology of neurodegeneration and dementia by proteomic profiling.
Review in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Effect of probiotics on cognitive function and cardiovascular risk factors in mild cognitive impairment and Alzheimer's disease: an umbrella meta-analysis.Journal of health, population, and nutrition · 2025Pooled it
- Evidence and Therapeutic Perspectives in the Relationship between the Oral Microbiome and Alzheimer's Disease: A Systematic Review.International journal of environmental research and public health · 2021Pooled it
- Spontaneous Non-Catalyzed Molecular Reactions and Interactions in the Human Body: Biomedical Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Mechanistic Role of Astrocytic Rac1 Protein in Alzheimer's Disease.Aging and disease · 2025Review
- Rhamnan Sulfate from the SeaweedMarine drugs · 2025Article
- Advances in Developing Small Molecule Drugs for Alzheimer's Disease.Current Alzheimer research · 2024Review
- Catalpol alleviates amyloid- generation and neuronal oxidative stress injury via activating the Keap1-Nrf2/ARE signaling pathway in the immortalized lymphocytes from patients with late-onset Alzheimer's disease and SKNMC cells co-culture model.Iranian journal of basic medical sciences · 2024Article
- Immunotherapy targeting isoDGR-protein damage extends lifespan in a mouse model of protein deamidation.EMBO molecular medicine · 2023Article
- Hydroxytyrosol-Donepezil Hybrids Play a Protective Role in an In Vitro Induced Alzheimer's Disease Model and in Neuronal Differentiated Human SH-SY5Y Neuroblastoma Cells.International journal of molecular sciences · 2023Article
- Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023Review
- Comparison of Oleocanthal-Low EVOO and Oleocanthal against Amyloid-β and Related Pathology in a Mouse Model of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Article
- The relationship between amyloid-beta and brain capillary endothelial cells in Alzheimer's disease.Neural regeneration research · 2022Review
- Relevance of plasma biomarkers to pathologies in Alzheimer's disease, Parkinson's disease and frontotemporal dementia.Scientific reports · 2022Article
- Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Risk of Dementia According to Surgery Type: A Nationwide Cohort Study.Journal of personalized medicine · 2022Article
- MEF2C ameliorates learning, memory, and molecular pathological changes in Alzheimer’s disease in vivo and in vitroActa biochimica et biophysica Sinica · 2022Article
- Progress Toward a Multiomic Understanding of Traumatic Brain Injury: A Review.Biomarker insights · 2022Review
- Molecular Pathways Involved in Frontotemporal Lobar Degeneration with TDP-43 Proteinopathy: What Can We Learn from Proteomics?International journal of molecular sciences · 2021Review
- Metabolomics Signatures of Aging: Recent Advances.Aging and disease · 2021Review
- Diverse proteins aggregate in mild cognitive impairment and Alzheimer's disease brain.Alzheimer's research & therapy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dementia is a syndrome associated with a wide range of clinical features including progressive cognitive decline and patient inability to self-care. Due to rapidly increasing prevalence in aging society, dementia now confers a major economic, social, and healthcare burden throughout the world, and has therefore been identified as a public health priority by the World Health Organization. Previous studies have established dementia as a 'proteinopathy' caused by detrimental changes in brain protein structure and function that promote misfolding, aggregation, and deposition as insoluble amyloid plaques. Despite clear evidence that pathological cognitive decline is associated with degenerative protein modifications (DPMs) arising from spontaneous chemical modifications to amino acid side chains, the molecular mechanisms that promote brain DPMs formation remain poorly understood. However, the technical challenges associated with DPM analysis have recently become tractable due to powerful new proteomic techniques that facilitate detailed analysis of brain tissue damage over time. Recent studies have identified that neurodegenerative diseases are associated with the dysregulation of critical repair enzymes, as well as the misfolding, aggregation and accumulation of modified brain proteins. Future studies will further elucidate the mechanisms underlying dementia pathogenesis via the quantitative profiling of the human brain proteome and associated DPMs in distinct phases and subtypes of disease. This review summarizes recent developments in quantitative proteomic technologies, describes how these techniques have been applied to the study of dementia-linked changes in brain protein structure and function, and briefly outlines how these findings might be translated into novel clinical applications for dementia patients. In this review, only spontaneous protein modifications such as deamidation, oxidation, nitration glycation and carbamylation are reviewed and discussed.
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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.