Alcohol can damage brain’s structural support — Study

A new study has found that alcohol can trigger immune cells in the brain to break down the structural support that helps nerve cells function, offering fresh insight into how heavy drinking may contribute to brain damage.

The study, published in the journal Immunity, found that alcohol activates microglia, immune cells that normally help protect the brain, prompting them to degrade the extracellular matrix (ECM), a network of molecules that provides structural support and helps regulate communication between brain cells.

The findings, based on experiments involving mice, suggest that alcohol’s effects on the brain may extend beyond its direct action on nerve cells to include changes in the brain’s immune system and surrounding tissue.

Researchers observed that microglia changed their shape and activity within about an hour of alcohol exposure, before the animals reached peak sedation.

Their branching extensions became shorter, reducing the area they could monitor. Repeated alcohol exposure worsened these changes, while the cells began engulfing and digesting components of the extracellular matrix.

The breakdown of this supportive network was associated with the loss of synaptic connections, which allow nerve cells to communicate with one another.

The researchers said the findings point to a possible pathway through which alcohol exposure could interfere with normal brain function.

According to the study, the research team used two-photon microscopy to observe changes in the brains of mice exposed to ethanol under conditions designed to model binge or heavy alcohol use.

The researchers also investigated the role of MyD88, a protein involved in immune signalling. When they genetically disabled MyD88 in the relevant cells, the mice showed less tissue damage and reduced sedation.

However, when the researchers used an enzyme to break down the extracellular matrix, synaptic loss, motor impairment and sedation returned. This suggested that damage to the matrix could contribute to some of the effects observed after alcohol exposure.

The study also examined brain tissue from six deceased people with alcohol use disorder. Compared with control samples, the tissue showed signs of disruption to the extracellular matrix.

However, the human findings were based on a small sample and do not establish that the same processes account for alcohol-related brain damage in people generally.

The researchers said the work could guide further investigations into how alcohol affects the brain and whether immune signalling pathways or protection of the extracellular matrix could offer potential targets for future treatment.

They stressed that further research is needed to establish how closely the findings from mice reflect the effects of alcohol exposure in humans.