title: Screening of innate immune receptors in neurodegenerative diseases: a similar pattern.
abstract: In Alzheimer's disease (AD), Parkinson's disease (PD), dementia with Lewy bodies (DLB) and amyotrophic lateral sclerosis (ALS), neuroinflammatory responses are considered to contribute to neuronal injury. Recently, the innate immune receptors, toll-like receptors (TLRs) and the LPS receptor (CD14) have been related to neurodegeneration. In this study, we systematically assessed the expression of most TLRs and CD14 in AD, PD/DLB and ALS using murine models of these diseases and human post-mortem brain tissues. A common upregulation of TLR2 and CD14 was found in all three animal models. While these two receptors could also be detected in AD patient tissues, they were absent from DLB and ALS tissues. This uniform pattern of innate immune response in animal models of neurodegenerative diseases clearly indicates that this response is part of a non-specific neuroinflammatory effector phase rather than a disease-specific event. The less dynamic disease progression in humans and the location (extracellular versus intracellular) of the aggregated proteins deposits might explain the divergent results seen between animal models and human tissues.
authors: University of the Saarland, Department of Neurology, Kirrberger Strasse, 66421 Homburg/Saar, Germany. m.letiembre@mx.uni-saarland.de
authors: Maryse
authors: M
authors: Letiembre
authors: Yang
authors: Y
authors: Liu
authors: Silke
authors: S
authors: Walter
authors: Wenlin
authors: W
authors: Hao
authors: Tatjana
authors: T
authors: Pfander
authors: Arne
authors: A
authors: Wrede
authors: Walter
authors: W
authors: Schulz-Schaeffer
authors: Klaus
authors: K
authors: Fassbender
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D000818:Animals; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001921:Brain / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004660:Encephalitis / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology; D045604:Extracellular Fluid / Q000276:immunology; D005260:Female; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D020961:Lewy Body Disease / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D018950:Lipopolysaccharide Receptors / Q000032:analysis / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology; D010300:Parkinson Disease / Q000235:genetics / Q000276:immunology / Q000503:physiopathology; D013045:Species Specificity; D051193:Toll-Like Receptors / Q000032:analysis / Q000378:metabolism*; D015854:Up-Regulation / Q000235:genetics / Q000276:immunology
chemical_list: D015415:Biomarkers; D018950:Lipopolysaccharide Receptors; D051193:Toll-Like Receptors