Antonietta Bernardo

TL;DR: The observations suggest that 15d‐PGJ2, the synthesis of which is likely to occur within the brain, could play an important role in preventing brain damage associated with excessive microglial activation.

TL;DR: The present review summarizes the several lines of evidence supporting that PPAR-gamma natural and synthetic agonists may control brain inflammation by inhibiting several functions associated to microglial activation, such as the expression of surface antigens and the synthesis of nitric oxide, prostaglandins, inflammatory cytokines and chemokines.

TL;DR: Recent findings supporting a major role for PPAR-γ agonists in controlling neuroinflammation and neurodegeneration through their activities on glial cells are reviewed, with a particular emphasis on microglial cells as major macrophage population of the brain parenchyma and main actors in brain inflammation.

TL;DR: Although required for cytoprotection, TRAF2 is not sufficient to protect cells from TNF + cycloheximide cytotoxicity when overexpressed in transfected cells, thus indicating an essential role of additional TNF receptor 1 complex components in the cy toprotective response.

TL;DR: It is shown that the R100 mutation selectively alters some of the signaling pathways activated downstream of TrkA NGF receptors, which means that proNGF has a significantly reduced nociceptive activity, with respect to NGF, and NGFR100 mutants maintain identical neurotrophic and neuroprotective properties.