Although some in vitro studies have suggested that ethanol can interfere with the BBB, most in vivo studies do not show BBB damage following chronic ethanol treatment. Marshall and colleagues (2013) assessed BBB integrity by tracking a protein (i.e., albumin) that cannot cross an intact BBB in rats that were administered large amounts of alcohol for 4 days (a regimen that can induce alcoholic brain damage). The analyses found no evidence of albumin in the brain, indicating that the BBB had remained intact following the ethanol treatment. Using the same model, Crews and colleagues (2006) found that inhibition of NF-κB protected against the brain damage and inhibition of neurogenesis normally induced by this regimen. These findings are consistent with the assumption that proinflammatory responses in the brain mediate brain damage without causing BBB damage. Instead, the brain damage may be induced through direct activation of proinflammatory responses in the brain and/or systemic proinflammatory signals that are transported across the BBB and contribute to brain proinflammatory responses.
