Human Cytokine Response to ex vivo Amyloid-β Stimulation is Mediated by Genetic Factors

Through its ability to induce the enhanced release and production of cytokines, amyloid-β is responsible for the chronic inflammatory response that contributes to Alzheimer's disease (AD). Determining whether the response of monocytes to amyloid-β stimulation is under genetic control may help u...

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Veröffentlicht in:	Twin research and human genetics 2005-04, Vol.8 (2), p.132-137
Hauptverfasser:	Posthuma, Danielle, Meulenbelt, Ingrid, de Craen, Anton J. M., de Geus, Eco J. C., Slagboom, P. Eline, Boomsma, Dorret I., Westendorp, Rudi G. J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Adolescent Adult Aged Alzheimer's disease Amyloid beta-Peptides - pharmacology Amyloid beta-protein Cytokines Cytokines - drug effects Cytokines - genetics Degeneration Diagnosis Environment Escherichia coli Female Genetic aspects Genetic control Genetic factors Genetic Variation - genetics Heritability Humans IL-1β Inflammation Interleukin 1 receptor antagonist Interleukin 1 receptors Interleukin 10 Interleukin 6 Interleukin-1 - genetics Interleukin-10 - genetics Interleukin-6 - genetics Lipopolysaccharides - pharmacology Male Middle Aged Monocytes Monocytes - drug effects Monocytes - metabolism Nervous system Neurodegenerative diseases Receptors, Interleukin-1 - antagonists & inhibitors Sex Factors Tumor Necrosis Factor-alpha - drug effects Tumor Necrosis Factor-alpha - genetics Twins, Dizygotic - genetics Twins, Monozygotic - genetics β-Amyloid
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