However, with the human adult brain, both age- and region-dependent effects of ethanol exposure have to be considered [51, 52]. A low grade pro-inflammatory phenotype has been shown to accompany aging in mammals, with a progressive disturbance of the interplay between autophagy and the inflammasome pathway [8]. Mitochondrial dysfunction and cortical spreading depression have been shown to follow ethanol abuse with aging [11]. Further studies should be performed in order to assess whether alcohol exposure in the adult human brain affects the mature or the neurogenic areas [15]. Additionally, the immunohistochemical analysis of the FASD human brain at the embryonic stage would provide additional information about ethanol-driven mechanisms from the pre-natal to the post-natal stage, including the participation of the inflammasome pathway in the early phase of FASD pathogenesis.
