ArticleThe Journal of biological chemistry2014
Analysis of the hippocampal proteome in ME7 prion disease reveals a predominant astrocytic signature and highlights the brain-restricted production of clusterin in chronic neurodegeneration.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Carbonic Anhydrase 3 Overexpression Modulates Signalling Pathways Associated with Cellular Stress Resilience and Proteostasis.International journal of molecular sciences · 2025Article
- Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease.Journal of neuroinflammation · 2023Article
- Chronic stress induces NPD-like behavior in APPPS1 and WT mice with subtle differences in gene expression.Genes, brain, and behavior · 2021Article
- The degree of astrocyte activation is predictive of the incubation time to prion disease.Acta neuropathologica communications · 2021Article
- Lack of the peroxiredoxin 6 gene causes impaired spatial memory and abnormal synaptic plasticity.Molecular brain · 2021Article
- Enhanced contextual fear memory in peroxiredoxin 6 knockout mice is associated with hyperactivation of MAPK signaling pathway.Molecular brain · 2021Article
- Unwanted Exacerbation of the Immune Response in Neurodegenerative Disease: A Time to Review the Impact.Frontiers in cellular neuroscience · 2021Review
- Molecular Investigation of the Unfolded Protein Response in Select Human Tauopathies.Journal of Alzheimer's disease reports · 2021Article
- 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
- Pathogenic tau does not drive activation of the unfolded protein response.The Journal of biological chemistry · 2019Article
- Re-transmissibility of mouse-adapted ME7 scrapie strain to ovine PrP transgenic mice.Journal of veterinary science · 2019Article
- Region-Specific Response of Astrocytes to Prion Infection.Frontiers in neuroscience · 2019Article
- Human stem cell-derived astrocytes replicate human prions in aThe Journal of experimental medicine · 2017Article
- Age and Environment Influences on Mouse Prion Disease Progression: Behavioral Changes and Morphometry and Stereology of Hippocampal Astrocytes.Oxidative medicine and cellular longevity · 2017Article
- Antioxidant peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo.Neurochemistry international · 2015Article
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- Proteomics analysis of amyloid and nonamyloid prion disease phenotypes reveals both common and divergent mechanisms of neuropathogenesis.Journal of proteome research · 2014Article
- Subtype and regional-specific neuroinflammation in sporadic creutzfeldt-jakob disease.Frontiers in aging neuroscience · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Prion diseases are characterized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal loss. This sequence, mirroring key features of Alzheimer disease, is modeled well in ME7 prion disease. We used iTRAQ(TM)/mass spectrometry to compare the hippocampal proteome in control and late-stage ME7 animals. The observed changes associated with reactive glia highlighted some specific proteins that dominate the proteome in late-stage disease. Four of the up-regulated proteins (GFAP, high affinity glutamate transporter (EAAT-2), apo-J (Clusterin), and peroxiredoxin-6) are selectively expressed in astrocytes, but astrocyte proliferation does not contribute to their up-regulation. The known functional role of these proteins suggests this response acts against protein misfolding, excitotoxicity, and neurotoxic reactive oxygen species. A recent convergence of genome-wide association studies and the peripheral measurement of circulating levels of acute phase proteins have focused attention on Clusterin as a modifier of late-stage Alzheimer disease and a biomarker for advanced neurodegeneration. Since ME7 animals allow independent measurement of acute phase proteins in the brain and circulation, we extended our investigation to address whether changes in the brain proteome are detectable in blood. We found no difference in the circulating levels of Clusterin in late-stage prion disease when animals will show behavioral decline, accumulation of misfolded protein, and dramatic synaptic and neuronal loss. This does not preclude an important role of Clusterin in late-stage disease, but it cautions against the assumption that brain levels provide a surrogate peripheral measure for the progression of brain degeneration.
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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.