The inflammasome of cytoplasmic receptor NALP3 was identified by Annett Halle and her colleagues from the University of Massachusetts (USA) as a sensor of amyloid-β in a process in which amyloid-β is phagocytosed, followed by lysosomal damage and the release of cathepsin B.

The fibrillar peptide amyloid-β is one of the key players in the pathogenesis of Morbus Alzheimer. Interleukin-1-β (IL-1b) is the main cytokine in the inflammatory response to amyloid-β. IL-1b is released when insoluble materials like crystals activate the NALP3 inflammasome.

The IL-1b pathway was also found to be required for the microglial product of proinflammatory and neurotoxic factors. Together with the inflammasome and caspase-1, IL-1b was of great importance for the recruitment of microglia to exogenoud amyloid-β in the brain.

The activation of the NALP3 inflammasome presents itself as responsible for inflammation and tissue damage in Morbus Alzheimer.

Related antibodies on antibodies-online.com:

Amyloid-β

Interleukin-1-β

NALP3

Cathepsin B

Caspase-1

Antibodies for the research area Morbus Alzheimer: »Show antibodies

Antibodies for the research area cytokines: »Show antibodies

Antibodies for the research area inflammation: »Show antibodies