ReviewTrends in neurosciences2006
Inducible proteopathies.
Review in Trends in neurosciences, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed.
- Review
- Current insights and assumptions on α-synuclein in Lewy body disease.Acta neuropathologica · 2024Review
- α-Synuclein seed amplification technology for Parkinson's disease and related synucleinopathies.Trends in biotechnology · 2024Review
- Uncovering supramolecular chirality codes for the design of tunable biomaterials.Nature communications · 2024Article
- Quantitation of Tissue Amyloid via Fluorescence Spectroscopy Using Controlled Concentrations of Thioflavin-S.Molecules (Basel, Switzerland) · 2023Article
- Protein Misfolding and Aggregation in Proteinopathies: Causes, Mechanism and Cellular Response.Diseases (Basel, Switzerland) · 2023Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- The Path to Progress Preclinical Studies of Age-Related Neurodegenerative Diseases: A Perspective on Rodent and hiPSC-Derived Models.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- Aged Cattle Brain Displays Alzheimer's Disease-Like Pathology and Promotes Brain Amyloidosis in a Transgenic Animal Model.Frontiers in aging neuroscience · 2021Article
- Identification of Molecular Signatures in Neural Differentiation and Neurological Diseases Using Digital Color-Coded Molecular Barcoding.Stem cells international · 2020Review
- Exfoliation Syndrome: A Disease of Autophagy and LOXL1 Proteopathy.Journal of glaucoma · 2018Review
- Critical appraisal of pathology transmission in the α-synuclein fibril model of Lewy body disorders.Experimental neurology · 2018Article
- Prion-like mechanisms in Alzheimer disease.Handbook of clinical neurology · 2018Review
- Article
- Mapping Neurodegenerative Disease Onset and Progression.Cold Spring Harbor perspectives in biology · 2017Review
- Parkinson's disease-associated receptor GPR37 is an ER chaperone for LRP6.EMBO reports · 2017Article
- Impact of lysosome status on extracellular vesicle content and release.Ageing research reviews · 2016Review
- PrP-containing aggresomes are cytosolic components of an ER quality control mechanism.Journal of cell science · 2016Article
- Astrocytes Surviving Severe Stress Can Still Protect Neighboring Neurons from Proteotoxic Injury.Molecular neurobiology · 2016Article
- Synergistic stress exacerbation in hippocampal neurons: Evidence favoring the dual-hit hypothesis of neurodegeneration.Hippocampus · 2016Article
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
Abstract
Numerous degenerative diseases are characterized by the aberrant polymerization and accumulation of specific proteins. These proteopathies include neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease and the prion diseases, in addition to diverse systemic disorders, particularly the amyloidoses. The prion diseases have been shown to be transmissible by an alternative conformation of the normal cellular prion protein. Other proteopathies have been thought to be non-transmissible, but there is growing evidence that some systemic and cerebral amyloidoses can be induced by exposure of susceptible hosts to cognate molecular templates. As we review here, the mechanistic similarities among these diseases provide unprecedented opportunities for elucidating the induction of protein misfolding and assembly in vivo, and for developing an integrated therapeutic approach to degenerative proteopathies.
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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.