TY  - JOUR
AU  - McManus, Róisín M.
AU  - Latz, Eicke
TI  - NLRP3 inflammasome signalling in Alzheimer's disease
JO  - Neuropharmacology
VL  - 252
SN  - 0028-3908
CY  - Amsterdam [u.a.]
PB  - Elsevier Science
M1  - DZNE-2024-00470
SP  - 109941
PY  - 2024
AB  - 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.
KW  - Animals
KW  - Humans
KW  - Alzheimer Disease: metabolism
KW  - Alzheimer Disease: immunology
KW  - Alzheimer Disease: drug therapy
KW  - Brain: metabolism
KW  - Brain: immunology
KW  - Inflammasomes: metabolism
KW  - NLR Family, Pyrin Domain-Containing 3 Protein: metabolism
KW  - NLR Family, Pyrin Domain-Containing 3 Protein: antagonists & inhibitors
KW  - Signal Transduction: physiology
KW  - Signal Transduction: drug effects
KW  - Alzheimer's disease (Other)
KW  - Immune-targeted therapies (Other)
KW  - Microglia (Other)
KW  - NLRP3 inflammasome (Other)
KW  - Neuroimmunology (Other)
KW  - Preclinical models (Other)
KW  - Inflammasomes (NLM Chemicals)
KW  - NLR Family, Pyrin Domain-Containing 3 Protein (NLM Chemicals)
KW  - NLRP3 protein, human (NLM Chemicals)
LB  - PUB:(DE-HGF)16
C6  - pmid:38565393
DO  - DOI:10.1016/j.neuropharm.2024.109941
UR  - https://pub.dzne.de/record/269039
ER  -