Recent NIA-funded research has revealed that inflammation may drive the development of tau tangles in Alzheimer’s disease (AD).  Abnormal neurofibrillary tangles of tau protein are one of the hallmark features of AD, along with beta-amyloid plaques.  While amyloid plaques have been linked with inflammatory changes in AD, the relationship between inflammation and tau pathology has not been fully understood.  In a study published in Nature, researchers used a mouse model to evaluate what would happen to tau proteins when an inflammasome, or a complex of proteins known to trigger inflammatory cascades, was “knocked out,” or rendered inactive.  The results revealed that blocking the action of the inflammasome NLRP3 prevented tau aggregation and tangling, which, in turn, led to better memory performance in the transgenic knockout mice.  The study also suggested that amyloid deposition and tau pathology are linked by the action of the inflammasome.  Therapies which block the inflammasome could reduce tauopathies (which are hypothesized to follow beta-amyloid deposition) and limit subsequent AD symptomatology.