Interleukin‐12/23 deficiency differentially affects pathology in male and female Alzheimer's disease‐like mice

Pathological aggregation of amyloid‐β (Aβ) is a main hallmark of Alzheimer's disease (AD). Recent genetic association studies have linked innate immune system actions to AD development, and current evidence suggests profound gender differences in AD pathogenesis. Here, we characterise gender‐sp...

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Veröffentlicht in:	EMBO reports 2020-03, Vol.21 (3), p.e48530-n/a
Hauptverfasser:	Eede, Pascale, Obst, Juliane, Benke, Eileen, Yvon‐Durocher, Genevieve, Richard, Bernhard C, Gimber, Niclas, Schmoranzer, Jan, Böddrich, Annett, Wanker, Erich E, Prokop, Stefan, Heppner, Frank L
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - genetics Alzheimer's disease Amyloid Amyloid beta-Peptides - metabolism Amyloid beta-Protein Precursor - metabolism Amyloidogenesis Amyloidosis Animals Brain Brain - metabolism Cytokines Disease Models, Animal EMBO19 EMBO24 EMBO27 Female Gender Gender aspects Gender differences Gliosis IL‐12/IL‐23 Immune system Innate immunity Interleukin 1 Interleukin-12 - deficiency Interleukin-12 - genetics Interleukin-12 Subunit p40 - deficiency Interleukin-12 Subunit p40 - genetics Interleukin-23 Subunit p19 - deficiency Interleukin-23 Subunit p19 - genetics Interleukins Male Mice Mice, Transgenic Neurodegenerative diseases Pathogenesis Pathology Plaque, Amyloid Rodents Sex differences Signaling β‐amyloid γ-Interferon
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