ReviewTrends in molecular medicine2011
The intricate mechanisms of neurodegeneration in prion diseases.
Review in Trends in molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis 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
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.
- Roles of neuropathology-associated reactive astrocytes: a systematic review.Acta neuropathologica communications · 2023Pooled it
- MGRN1 in development and disease: a unifying view of a versatile membrane-tethered E3 ubiquitin ligase.Biochemical Society transactions · 2026Review
- OPA1 Requires ATP Synthase Activity and Oligomerization to Mitigate Prion-Induced Mitochondrial Dysfunction, Oxidative Stress, and Neuronal Apoptosis.Molecular neurobiology · 2026Article
- Copper Coordination to the Prion Fragment (95-126): Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2026Article
- Bovine Spongiform Encephalopathy: An Integrated Review of Prion Mechanisms, Neuroanatomy, and Control.Veterinary sciences · 2026Review
- PrPEnvironmental science & technology · 2026Article
- The Anti-Apoptotic Activity of β-Synuclein Mediated via Akt Signaling Is Severely Lost During Prion Infection.International journal of molecular sciences · 2026Article
- Modelling human proteostasis and organelle homeostasis disorders in yeast and its application in drug discovery.FEMS yeast research · 2026Review
- Discovering, Integrating, and Reinterpreting the Molecular Logic of Life: From Classical Theories of Heredity to an Extended Functional Perspective on the Central Dogma.Life (Basel, Switzerland) · 2026Review
- Time-dependent transcriptomic response to scrapie exposure in ovine MSC-derived neuron-like cells.Frontiers in cellular and infection microbiology · 2026Article
- A Drosophila model of prion disease and its metabolic changes in the brain.Animal models and experimental medicine · 2025Article
- The Role of Prion Protein in Reelin/Dab1 Signaling: Implications for Neurodegeneration.Viruses · 2025Article
- 'Intelligent' proteins.Cellular and molecular life sciences : CMLS · 2025Review
- Prion replication in organotypic brain slice cultures is distinct from in vivo inoculation and is species dependent.Acta neuropathologica communications · 2025Article
- Role of Antioxidants in Modulating the Microbiota-Gut-Brain Axis and Their Impact on Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Inhibition of amyloid formation of prion fragment (106-128) by polyphenolic compounds.Biochimica et biophysica acta. General subjects · 2025Article
- Biological characteristics and transcriptomic profile of adipose-derived mesenchymal stem cells isolated from prion-infected murine model.Stem cell research & therapy · 2025Article
- High cellular prion protein expression in cholangiocarcinoma: A marker for early postoperative recurrence and unfavorable prognosis.World journal of gastrointestinal surgery · 2025Article
- A novel ER stress regulator ARL6IP5 induces reticulophagy to ameliorate the prion burden.Autophagy · 2025Article
- Evidence Suggesting That Alzheimer's Disease May Be a Transmissible Disorder.International journal of molecular sciences · 2025Article
34 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Prion diseases are a group of infectious neurodegenerative diseases with an entirely novel mechanism of transmission, involving a protein-only infectious agent that propagates the disease by transmitting protein conformational changes. The disease results from extensive and progressive brain degeneration. The molecular mechanisms involved in neurodegeneration are not entirely known but involve multiple processes operating simultaneously and synergistically in the brain, including spongiform degeneration, synaptic alterations, brain inflammation, neuronal death and the accumulation of protein aggregates. Here, we review the pathways implicated in prion-induced brain damage and put the pieces together into a possible model of neurodegeneration in prion disorders. A more comprehensive understanding of the molecular basis of brain degeneration is essential to develop a much needed therapy for these devastating diseases.
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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.