Acetyl-L-carnitine protects the brain from alcohol-induced damage

Alcohol in excess is a significant promoter of accelerated neurodegeneration. The authors of a welcome paper recently published in Free Radical Biology and Medicine first elucidate the...

"...cellular and biochemical mechanisms of alcohol-induced oxidative damage in different types of brain cells."

Interestingly, alcohol administration generated increased levels of reactive oxygen species ('free radicals') localized mainly in the astrocytes and microglia ('housekeeper' immune cells in the brain). As a result,

"Oxidative damage in glial cells was accompanied by their pronounced activation (astrogliosis) and coincident neuronal loss, suggesting that inflammation in glial cells caused neuronal degeneration."

In other words, the oxidative stress induced by alcohol resulted in an autoimmune inflammatory attack on brain tissue. But here's the good news:

"Co-administration of ALC [acetyl-L-carnitine] with alcohol showed a significant reduction in oxidative damage, neuronal loss and a restoration of synaptic neurotransmission in this brain region, suggesting that ALC protects brain cells from ethanol-induced oxidative injury. These findings suggest the potential clinical utility of ALC as a neuroprotective agent that prevents alcohol-induced brain damage and development of neurological disorders."