Inflammasome: a new trigger of Alzheimer's disease.

Tara Saco,Narasaiah Kolliputi,Richard F Lockey,Prasanna T Parthasarathy,Young Cho

doi:10.3389/fnagi.2014.00080

Tara Saco, Narasaiah Kolliputi + Show 3 more

Open Access

https://doi.org/10.3389/fnagi.2014.00080

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Abstract

Inflammasome: a new trigger of Alzheimer's disease.

Highlights

Edited by: Fernanda Laezza, University of Texas Medical Branch, USA Reviewed by: Fernanda Laezza, University of Texas Medical Branch, USA Filippo Tempia, University of Turin, Italy
The researchers examined the differences in the level of spatial memory impairment between these groups and found that in amyloid precursor protein (APP)/PS1/NLRP3−/− and APP/PS1/Casp-1−/− mice, the level of cleaved Casp-1 was markedly decreased when compared to APP/PS1 mice, while IL-1β levels were consistent between the groups (Heneka et al, 2013)
The researchers compared the level of long-term potentiation (LTP), which is analogous to synaptic plasticity, in the hippocampi of these mice

Summary

Introduction

Edited by: Fernanda Laezza, University of Texas Medical Branch, USA Reviewed by: Fernanda Laezza, University of Texas Medical Branch, USA Filippo Tempia, University of Turin, Italy. NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice by Heneka, M. The main contributing factor in the development of Alzheimer’s disease is the deposition of β-amyloid in the brain, especially in the hippocampus (Heneka et al, 2013).

Results

Conclusion