Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Atypical inflammation in the central nervous system in prion disease

1 Jun 2002

Abstract excerpt

The inflammatory response in prion diseases is dominated by microglial activation. Contrary to their profile in vitro none of the pro-inflammatory cytokines interleukin-1beta, interleukin-6, or tumour necrosis factor-alpha are significantly upregulated in the ME7 model of prion disease. However, two major inflammatory mediators are elevated: transforming growth factor-beta1 and prostaglandin E2. This cytokine...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer's disease research and treatments
Share to Nuclear Receptors and Signaling
Share to Prion Diseases and Protein Misfolding

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 12045736
DOI: 10.1097/00019052-200206000-00020

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Atypical inflammation in the central nervous system in prion diseasePMID 12045736Read ↗

Microglia in prion diseases.Semantic proximity Read ↗

Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype.Semantic proximity Read ↗

Systemic Inflammation Accelerates Changes in Microglial and Synaptic Markers in an Experimental Model of Chronic NeurodegenerationSemantic proximity Read ↗

Microglia in the degenerating brain are capable of phagocytosis of beads and of apoptotic cells, but do not efficiently remove PrPSc, even upon LPS stimulation.Semantic proximity Read ↗

The impact of neuroimmune changes on development of amyloid pathology; relevance to Alzheimer's disease.Semantic proximity Read ↗

LPS-induced systemic inflammation reveals an immunomodulatory role for the prion protein at the blood-brain interface.Semantic proximity Read ↗

Prion pathogenesis is unaltered in the absence of SIRPα-mediated "don't-eat-me" signaling.Semantic proximity Read ↗

Modelling neuroinflammatory phenotypes in vivo.Semantic proximity Read ↗

Inflammatory response in the hippocampus of PS1M146L/APP751SL mouse model of Alzheimer's disease: age-dependent switch in the microglial phenotype from alternative to classic.Semantic proximity Read ↗

Prion Infection of Mouse Brain Reveals Multiple New Upregulated Genes Involved in Neuroinflammation or Signal TransductionSemantic proximity Read ↗

The role of innate and adaptive immunity in Parkinson's disease.Semantic proximity Read ↗

Sex and APOE Genotype Alter the Basal and Induced Inflammatory States of Primary Microglia from APOE Targeted Replacement Mice.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.