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Rodney Johnson"Inflammation gets into brains of aged subjects: Evidence and functional consequences".

Abstract :

n the healthy adult brain, there is a balance between pro-inflammatory and anti-inflammatory mediators, with microglial cells remaining quiescent. However, in chronic neurodegenerative diseases, microglia can be transformed to a “primed” or activated state Both primed and activated microglia are de-ramified and express morphological markers that suggest activation including MHC class II and complement receptors, but only activated microglia produce appreciable levels of inflammatory cytokines. Primed microglial cells, however, are hyper-responsive to secondary stimuli and thus can produce an exaggerated cytokine response when provoked by the peripheral innate immune system.

This lecture will focus on a new hypothesis that suggests normal aging primes microglial cells for an exaggerated inflammatory response when the peripheral innate immune system is activated. Results from a recent study in an aged mouse model that showed exaggerated neuroinflammation and sickness behavior after activation of the peripheral innate immune system will be presented, and the importance of this dysregulated link between the peripheral immune system and brain to severe behavioral deficits that frequently occur in older adults with systemic infections will be discussed.

Selected publications

J Neuroimmunol. 2005 Sep 5;
alpha-Tocopherol attenuates NFkappaB activation and pro-inflammatory cytokine production in brain and improves recovery from lipopolysaccharide-induced sickness behavior.
Godbout JP, Berg BM, Krzyszton C, Johnson RW.

Robert Dantzer