2. Academic Validation
  3. NLRP3 inflammasome signalling in Alzheimer's disease

NLRP3 inflammasome signalling in Alzheimer's disease

  • Neuropharmacology. 2024 Jul 1:252:109941. doi: 10.1016/j.neuropharm.2024.109941.
Róisín M McManus 1,  Eicke Latz 2
Affiliations

Affiliations

  • 1 German Center for Neurodegenerative Diseases (DZNE), Venusberg Campus 1/99, 53127, Bonn, Germany; Institute of Innate Immunity, University Hospital Bonn, Bonn, Germany. Electronic address: roisin.mcmanus@dzne.de.
  • 2 Institute of Innate Immunity, University Hospital Bonn, Bonn, Germany; Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, 7491, Trondheim, Norway; Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, 01605, USA; Deutsches Rheuma-Forschungszentrum (DRFZ), Charitéplatz 1, 10117, Berlin, Germany.
PMID: 38565393 DOI: 10.1016/j.neuropharm.2024.109941
Abstract

Every year, 10 million people develop dementia, the most common of which is Alzheimer's disease (AD). To date, there is no way to prevent cognitive decline and therapies are limited. This review provides a neuroimmunological perspective on the progression of AD, and discusses the immune-targeted therapies that are in preclinical and clinical trials that may impact the development of this disease. Specifically, we look to the role of the NLRP3 inflammasome, its triggers in the brain and how its activation can contribute to the progression of dementia. We summarise the range of inhibitors targeting the NLRP3 inflammasome and its downstream pathways that are under investigation, and discuss future therapeutic perspectives for this devastating condition.

Keywords

Alzheimer's disease; Immune-targeted therapies; Microglia; NLRP3 inflammasome; Neuroimmunology; Preclinical models.

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