ArticleThe Journal of clinical investigation2013
Thinking laterally about neurodegenerative proteinopathies.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06528964 (Expression of Proteinopathies in Skin Biopsies of Patients With Neurodegenerative Disorders), which is not on this map. Cited by 70 papers.
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.
Expression of Proteinopathies in Skin Biopsies of Patients With Neurodegenerative Disorders
Who cites it
70 citing papers in PubMed.
- Safety and Tolerability of Active Immunotherapy Targeting α-Synuclein with PD03A in Patients with Early Parkinson's Disease: A Randomized, Placebo-Controlled, Phase 1 Study.Journal of Parkinson's disease · 2021Trial
- The default mode network exhibits circuit-specific selective vulnerability despite widespread amyloid burden in an animal model of Alzheimer's disease.Nature communications · 2026Article
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.Nature communications · 2025Article
- SON-dependent nuclear speckle rehabilitation alleviates proteinopathies.bioRxiv : the preprint server for biology · 2025Article
- PET tracer development for imaging α-synucleinopathies.Archives of pharmacal research · 2025Review
- Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.Acta neuropathologica · 2025Article
- Tremendous Fidelity of Vitamin D3 in Age-related Neurological Disorders.Molecular neurobiology · 2024Review
- TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy.bioRxiv : the preprint server for biology · 2024Article
- MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model.Molecular neurobiology · 2024Article
- Vcp overexpression and leucine supplementation extend lifespan and ameliorate neuromuscular junction phenotypes of a SOD1G93A-ALS mouse model.Human molecular genetics · 2024Article
- Emerging role of senescent microglia in brain aging-related neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Evidence for ~12-h ultradian gene programs in humans.Npj biological timing and sleep · 2024Article
- New Insights into the Relationship between Nutrition and Neuroinflammation in Alzheimer's Disease: Preventive and Therapeutic Perspectives.CNS & neurological disorders drug targets · 2024Review
- Review
- Neuromodulatory effect of vardenafil on aluminium chloride/D-galactose induced Alzheimer's disease in rats: emphasis on amyloid-beta, p-tau, PI3K/Akt/p53 pathway, endoplasmic reticulum stress, and cellular senescence.Inflammopharmacology · 2023Article
- Treatment of Alzheimer's Disease: Beyond Symptomatic Therapies.International journal of molecular sciences · 2023Review
- Molecular Tweezers: Supramolecular Hosts with Broad-Spectrum Biological Applications.Pharmacological reviews · 2023Review
- Microglia phenotypes are associated with subregional patterns of concomitant tau, amyloid-β and α-synuclein pathologies in the hippocampus of patients with Alzheimer's disease and dementia with Lewy bodies.Acta neuropathologica communications · 2022Article
- Alzheimer's disease - the journey of a healthy brain into organ failure.Molecular neurodegeneration · 2022Review
- Alzheimer's disease and progressive supranuclear palsy share similar transcriptomic changes in distinct brain regions.The Journal of clinical investigation · 2022Article
10 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, Huntington's disease, and frontotemporal dementia, are proteinopathies that are associated with the aggregation and accumulation of misfolded proteins. While remarkable progress has been made in understanding the triggers of these conditions, several challenges have hampered the translation of preclinical therapies targeting pathways downstream of the initiating proteinopathies. Clinical trials in symptomatic patients using therapies directed toward initiating trigger events have met with little success, prompting concerns that such therapeutics may be of limited efficacy when used in advanced stages of the disease rather than as prophylactics. Herein, we discuss gaps in our understanding of the pathological processes downstream of the trigger and potential strategies to identify common features of the downstream degenerative cascade in multiple CNS proteinopathies, which could potentially lead to the development of common therapeutic targets for multiple disorders.
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.