Sustained interleukin-1β overexpression exacerbates tau pathology despite reduced amyloid burden in an Alzheimer's mouse model

Neuroinflammation is an important component of Alzheimer's disease (AD) pathogenesis and has been implicated in neurodegeneration. Interleukin-1 (IL-1), a potent inflammatory cytokine in the CNS, is chronically upregulated in human AD and believed to serve as part of a vicious inflammatory cycl...

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Veröffentlicht in:	The Journal of neuroscience 2013-03, Vol.33 (11), p.5053-5064
Hauptverfasser:	Ghosh, Simantini, Wu, Michael D, Shaftel, Solomon S, Kyrkanides, Stephanos, LaFerla, Frank M, Olschowka, John A, O'Banion, M Kerry
Format:	Artikel
Sprache:	eng
Schlagworte:	Age Factors Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - genetics Amyloid Precursor Protein Secretases - metabolism Analysis of Variance Animals Brain - metabolism Brain - pathology Disease Models, Animal Enzyme-Linked Immunosorbent Assay Gene Expression Regulation - genetics Glial Fibrillary Acidic Protein - metabolism Glycogen Synthase Kinase 3 - metabolism Humans Immunodeficiency Virus, Feline - genetics Interleukin-1beta - deficiency Interleukin-1beta - metabolism MAP Kinase Signaling System Mice Mice, Inbred C57BL Microfilament Proteins Muscle Proteins Mutation - genetics Presenilin-1 - genetics tau Proteins - genetics tau Proteins - metabolism Trisaccharides - metabolism Tubulin - metabolism
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