ArticlePloS one2013
Early Hippocampal Synaptic Loss Precedes Neuronal Loss and Associates with Early Behavioural Deficits in Three Distinct Strains of Prion Disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 59 citations in OpenAlex.
- Aquaporin-4 mislocalization from astrocyte endfeet prolongs survival in a prion-cerebral amyloid angiopathy model.bioRxiv : the preprint server for biology · 2026Article
- PrPStem cell reports · 2026Article
- Distinct cerebrospinal fluid proteomic signatures define clinicopathological subtypes of sporadic Creutzfeldt-Jakob disease and predict patient survival.Acta neuropathologica communications · 2025Article
- Stereotaxic Delivery of M1000 Prions to the Hippocampus Induces Related Behavioural and Cognitive Changes Consistent with Acute Neurotoxic Effects.Molecular neurobiology · 2025Article
- Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice.The Journal of clinical investigation · 2025Article
- Distinct patterns of prion strain deposition and toxicity in a novel whole brain organotypic slice culture system.Scientific reports · 2025Article
- Reactive Microglia and Astrocytes as Therapeutic Targets in Prion Diseases.Sub-cellular biochemistry · 2025Review
- TREM2 supports neuronal protection and microglial reactivity without an effect on misfolded protein deposition in chronic neurodegenerative prion disease.Frontiers in neuroscience · 2025Article
- Limbic system synaptic dysfunctions associated with prion disease onset.Acta neuropathologica communications · 2024Article
- 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
- Diagnosis in Scrapie: Conventional Methods and New Biomarkers.Pathogens (Basel, Switzerland) · 2023Review
- Diagnostic and prognostic value of cerebrospinal fluid SNAP-25 and neurogranin in Creutzfeldt-Jakob disease in a clinical setting cohort of rapidly progressive dementias.Alzheimer's research & therapy · 2023Article
- Prions induce an early Arc response and a subsequent reduction in mGluR5 in the hippocampus.Neurobiology of disease · 2022Article
- Neurogranin and Neurofilament Light Chain as Preclinical Biomarkers in Scrapie.International journal of molecular sciences · 2022Article
- Quantification of the trans-synaptic partners neurexin-neuroligin in CSF of neurodegenerative diseases by parallel reaction monitoring mass spectrometry.EBioMedicine · 2022Article
- Non-cell autonomous astrocyte-mediated neuronal toxicity in prion diseases.Acta neuropathologica communications · 2021Article
- Systemic Inflammation Accelerates Changes in Microglial and Synaptic Markers in an Experimental Model of Chronic Neurodegeneration.Frontiers in neuroscience · 2021Article
- Unwanted Exacerbation of the Immune Response in Neurodegenerative Disease: A Time to Review the Impact.Frontiers in cellular neuroscience · 2021Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Region-specific glial homeostatic signature in prion diseases is replaced by a uniform neuroinflammation signature, common for brain regions and prion strains with different cell tropism.Neurobiology of disease · 2020Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Prion diseases are fatal neurodegenerative diseases of the CNS that are associated with the accumulation of misfolded cellular prion protein. There are several different strains of prion disease defined by different patterns of tissue vacuolation in the brain and disease time course, but features of neurodegeneration in these strains have not been extensively studied. Our previous studies using the prion strains ME7, 79A and 22L showed that infected mice developed behavioural deficits in the same sequence and temporal pattern despite divergent end-stage neuropathology. Here the objective was to address the hypothesis that synaptic loss would occur early in the disease in all three strains, would precede neuronal death and would be associated with the early behavioural deficits. C57BL/6 mice inoculated with ME7, 79A, or 22L-infected brain homogenates were behaviourally assessed on species typical behaviours previously shown to change during progression and euthanised when all three strains showed statistically significant impairment on these tasks. A decrease in labelling with the presynaptic marker synaptophysin was observed in the stratum radiatum of the hippocampus in all three strains, when compared to control animals. Negligible cell death was seen by TUNEL at this time point. Astrocyte and microglial activation and protease resistant prion protein (PrP(Sc)) deposition were assessed in multiple brain regions and showed some strain specificity but also strongly overlapping patterns. This study shows that despite distinct pathology, multiple strains lead to early synaptic degeneration in the hippocampus, associated with similar behavioural deficits and supports the idea that the initiation of synaptic loss is a primary target of the misfolded prion agent.
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