| dc.description.abstract | Alzheimer’s disease (AD) is an age-related, neurodegenerative disease that results in memory loss, behavior and personality changes, as well as a decrease in
thinking abilities. Among tissue manifestations is included the generation of amyloid plaques into the extracellular brain parenchyma composed by amyloid β (Aβ) peptide 1.
Although Aβ-neurotoxicity involves activation of NMDA receptors, sustained elevations of [Ca2+]i, and oxidative stress (Laferla et al., 2007), the full underlying mechanism
associated to AD remains to be elucidated. Cerebral cortex and hippocampus from AD patients exhibit a reactive gliosis characterized by activated microglia and astrocytes
closely associated with amyloid plaques (Kalaria et al., 1999). It has been noted that the immunoreactivity of Cx43 is increased around amyloid plaques where reactive gliosis
occurs (Nagy et al., 1996). The present partnership has already shown that under chronic pathological threatening conditions (e.g., AD) microglia become overactivated
and release TNF-α and IL-β two pro-inflammatory molecules that increase HC opening and reduce gap junctional communication in astrocytes, depriving neurons of glial
protective functions and further reducing neuronal viability (Orellana et al., 2009). In addition, the cytokine-induced astroglial hemichannel activity is prevented by
cannabinoids (Froger et al., 2009), which have been shown to reduce the Aβ- induced neuroinflammation in vivo (Esposito et al., 2007). Indeed, cannabinoids are good
candidates to reduce the inflammatory response and gliosis (Cabral and Griffin-Thomas, 2008; Croxford, 2003) and because astrocytes and MG are one of their targets
in the central nervous system (Stella, 2004). Increasing number of studies revealed the anti-inflammatory properties of CBs are exerted both in periphery and in CNS (for
reviews see Klein et al.. 2003, Klein. 2005; Pacher et al., 2006; Walter and Stella, 2004; | |
