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University of Illinois at Chicago researchers has found some of the genes affected by alcohol and inflammation are also implicated in processes that clear amyloid beta-the protein that forms globs of plaques in the brain and contributes to neuronal damage and the cognitive impairment associated with Alzheimer’s disease.
Previous studies investigating the effects of alcohol consumption on Alzheimer’s disease have been controversial-some have indicated that alcohol has a protective effect, while others have pointed to a deleterious role for alcohol in the development of this neurocognitive disease.
Recent research has suggested that alcohol consumption, and its impact on the immune system and inflammation in the brain, may be the reason why alcohol might exert its influence on the development of Alzheimer’s disease. Dr. Douglas Feinstein, professor of anesthesiology in the University of Illinois at Chicago College of Medicine, and other researchers conducted a cell-based study which suggests that alcohol may impede the clearance of amyloid beta in the brain.
Researchers wanted to determine genes that are affected by both alcohol and high levels of inflammation in microglial cells. These are cells that support neural cells in the brain and other parts the body. One of their functions is to engulf and digest the amyloid beta protein plaques characteristic of Alzheimer’s disease in a process known as phagocytosis. Microglial cells are also known to express high levels of inflammatory markers due to chronic alcohol exposure.
Researchers exposed rat microglial cells to alcohol, pro-inflammatory chemicals called cytokines, or alcohol and cytokines in the lab for 24 hours, and looked at changes in gene expression under each condition. They also looked at the impact of alcohol exposure on the cells’ ability to engulf amyloid beta. They found that gene expression was altered for 312 genes under the alcohol condition; for 3,082 for the pro-inflammatory condition, and 3,552 for the alcohol and pro-inflammatory condition.
Changes in gene expression-either an increase or decrease in expression compared to normal levels-averaged about 16 percent and ranged from a 50 percent decrease to a 72 percent increase. Just a handful of genes were involved in both phagocytosis and inflammation.
The results suggest that alcohol impedes the ability of mircroglia to keep the brain clear of amyloid beta and may contribute to the development of Alzheimer’s disease. Exposing the cells to alcohol levels at doses that are comparable to those found in humans after binge drinking or in heavy drinkers, makes microglial phagocytosis significantly suppressed by about 15 percent after one hour.
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