ArticlePLoS pathogens2022
Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Advances in Single-Cell Sequencing for Infectious Diseases: Progress and Perspectives.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Downregulation of STAT3 transcription factor reverses synaptotoxic phenotype of reactive astrocytes associated with prion diseases.Acta neuropathologica communications · 2025Article
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- Human Genetic Evidence for New Targets in Prion Diseases: Opportunities and Challenges.Sub-cellular biochemistry · 2025Review
- Single-cell transcriptomics unveils molecular signatures of neuronal vulnerability in a mouse model of prion disease that overlap with Alzheimer's disease.Nature communications · 2024Article
- Prion diseases disrupt glutamate/glutamine metabolism in skeletal muscle.PLoS pathogens · 2024Article
- Reactive astrocytes in prion diseases: Friend or foe?PLoS pathogens · 2024Review
- Translatome and transcriptome profiling of neonatal mice hippocampus exposed to sevoflurane anesthesia.Heliyon · 2024Article
- Anti-prion drugs do not improve survival in novel knock-in models of inherited prion disease.PLoS pathogens · 2024Article
- Selective Vulnerability to Neurodegenerative Disease: Insights from Cell Type-Specific Translatome Studies.Biology · 2024Review
- Etiology matters: genetic and acquired prion diseases engage different mechanisms at a presymptomatic stage.Neural regeneration research · 2023Article
- Reactive astrocytes associated with prion disease impair the blood brain barrier.Neurobiology of disease · 2023Article
- Reactive astrocytes associated with prion disease impair the blood brain barrier.bioRxiv : the preprint server for biology · 2023Article
- Therapeutic Trial of anle138b in Mouse Models of Genetic Prion Disease.Journal of virology · 2023Article
- Cerebellar granule neurons induce Cyclin D1 before the onset of motor symptoms in Huntington's disease mice.Acta neuropathologica communications · 2023Article
- Dysregulation of neuroprotective astrocytes, a spectrum of microglial activation states, and altered hippocampal neurogenesis are revealed by single-cell RNA sequencing in prion disease.Acta neuropathologica communications · 2022Article
- Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons.Life science alliance · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selective vulnerability is an enigmatic feature of neurodegenerative diseases (NDs), whereby a widely expressed protein causes lesions in specific cell types and brain regions. Using the RiboTag method in mice, translational responses of five neural subtypes to acquired prion disease (PrD) were measured. Pre-onset and disease onset timepoints were chosen based on longitudinal electroencephalography (EEG) that revealed a gradual increase in theta power between 10- and 18-weeks after prion injection, resembling a clinical feature of human PrD. At disease onset, marked by significantly increased theta power and histopathological lesions, mice had pronounced translatome changes in all five cell types despite appearing normal. Remarkably, at a pre-onset stage, prior to EEG and neuropathological changes, we found that 1) translatomes of astrocytes indicated reduced synthesis of ribosomal and mitochondrial components, 2) glutamatergic neurons showed increased expression of cytoskeletal genes, and 3) GABAergic neurons revealed reduced expression of circadian rhythm genes. These data demonstrate that early translatome responses to neurodegeneration emerge prior to conventional markers of disease and are cell type-specific. Therapeutic strategies may need to target multiple pathways in specific populations of cells, early in disease.
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.