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Genetic variability in response to Amyloid beta deposition influences Alzheimer's disease risk

ABSTRACT: Genetic variability in response to Amyloid beta deposition influences Alzheimer's disease risk

PROVIDER: PRJNA565147 | ENA |

REPOSITORIES: ENA

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Genetic variability in response to Amyloid beta deposition influences Alzheimer's disease risk

Project description:The purpose of this project was to compare whole genome expression in 5 transgenic mice that show either amyloid plaques or tangle pathology to the expression in wild-type control mice at different stages of disease progression (2, 4, 8 or 18 months of age). Mouse genes with expression correlating to pathology were then compared to human genes showing DNA variation in human population associated with dementia (from GWAS).

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Genetic variability in response to amyloid beta deposition influences Alzheimer's disease risk.

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Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease Microglia were FACS-purified from 8.5 month old WT, Trem2-/-, 5XFAD, and Trem2-/- 5XFAD mice

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Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

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Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease

Project description:Alzheimer's disease (AD) is the most common neurodegenerative disorder affecting memory and cognition. The disease is accompanied by an abnormal deposition of ß-amyloid plaques in the brain that contributes to neurodegeneration and is known to induce glial inflammation. Studies in the APP/PS1 mouse model of ß-amyloid-induced neuropathology have suggested a role for inflammasome activation in ß-amyloid-induced neuroinflammation and neuropathology. Here, we evaluated the in vivo role of microglia-selective and full body inflammasome signalling in several mouse models of ß-amyloid-induced AD neuropathology. Unexpectedly, microglia-specific deletion of the inflammasome regulator A20 and inflammasome effector protease caspase-1 in the AppNL-G-F and APP/PS1 models failed to identify a prominent role for microglial inflammasome signalling in ß-amyloid-induced neuropathology. Moreover, global inflammasome inactivation through respectively full body deletion of caspases 1 and 11 in AppNL-G-F mice and Nlrp3 deletion in APP/PS1 mice, also failed to modulate amyloid pathology and disease progression. In agreement, single-cell RNA sequencing did not reveal an important role for Nlrp3 signalling in driving microglial activation and the transition into disease-associated states, both during homeostasis and upon amyloid pathology. Collectively, these results question a generalizable role for inflammasome activation in pre-clinical amyloid-only models of neuroinflammation.

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Microarray analysis on human neuroblastoma cells exposed to iron, B-amyloid or the B-amyloid iron complex

Project description:Microarray analysis on human neuroblastoma cells exposed to iron, B-amyloid or the B-amyloid iron complex. Alzheimer's disease is associated with an abnormal accumulation of certain metal ions.

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Increased neutrophils in inflammatory bowel disease accelerate the accumulation of amyloid plaques in the mouse model of Alzheimer's disease

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Plasmin activity promotes amyloid deposition in a new transgenic model of human transthyretin amyloidosis.

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