Neuroinflammation is common to various diseases of the central nervous system (CNS). It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity, but its imprecise definition has led to many misconceptions in research and clinical approaches. It is now recognized that neuroinflammation in chronic neurodegenerative conditions, including Alzheimer's disease (AD) and age-related dementia, is distinct from the inflammation that for example accompanies relapsing-remitting multiple sclerosis (RRMS). Several studies have pointed to the existence of inflammasome-mediated inflammatory pathways in central nervous system (CNS) disorders and associated changes in behavior. Neuroinflammation is mediated by the protein complexes known as inflammasomes.
In a recent publication* on inflammasomes and innate immunity in Alzheimer's disease, new data from genetics, clinical imaging and animal testing suggests mutual interaction of innate immune mechanisms and neurodegenerative processes. The key components for the congenital immune response observed in Alzheimer's patient brain, are the NOD-like receptor (NLR) family, pyrin domain containing 3 and 1 inflammasomes present in myeloid cells and neurons. Cell culture and animal models of Alzheimer's disease have shown that inhibition of inflammasome activation could be beneficial and protective against cognitive deficits and neuron death, opening new ways for therapeutic intervention.
*Heneka, MT. Inflammasome activation and innate immunity in Alzheimer's disease. Brain Pathol. 2017, 27(2), 220-222