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A study published in "Nature-Metabolism", Brain ethanol metabolism by astrocytic ALDH2 drives the behavioural effects of ethanol intoxication, showed that in mice, alcoholism may affect the behavior of the brain rather than the alcohol breakdown products (metabolites) produced by the brain rather than the liver.
)caused.
This result provides new insights into how alcohol may affect the brain, and is expected to be used to better regulate the effects of alcohol on behavior.
The effects of alcohol on human and mouse behavior (such as motor dysfunction) are thought to be caused by metabolites produced during the breakdown of alcohol.
One of the metabolites is acetate, which is produced by acetaldehyde dehydrogenase 2 (ALDH2), which is abundant in the liver.
Acetate produced by the liver will reach the brain through the bloodstream, where it impairs motor function through the signal transduction of the inhibitory neurotransmitter GABA.
Li Zhang of the National Institute of Alcohol Abuse and Poisoning in Bethesda, Maryland, USA, and colleagues observed this phenomenon in three human brain samples and 11 mice.
ALDH2 is expressed in the astrocytes of the cerebellum-the cerebellum It is the brain area that controls balance and motor coordination.
When ALDH2 was removed from the astrocytes of the cerebellum, the mice did not develop motor dysfunction caused by alcohol intake.
In general, alcohol intake will increase the levels of acetate and GABA in the brain, but removing ALDH2 in astrocytes can prevent this level of increase.
In contrast, removing ALDH2 from the liver failed to affect the levels of acetate or GABA in the brain.
The above research results show that the ability of acetate produced by the brain and liver to affect motor function is different.
The authors concluded that alcohol metabolism may be directly regulated in the brain, and it is expected to discover new targets for altering the effects of alcohol and treat alcohol use disorders.
However, further research is needed to determine whether these mechanisms observed in mice also exist in humans.
ALDH2 in astrocytes selectively regulates acetate produced by alcohol metabolism in cerebellar tissue.
Picture from Zhang et al.
©Nature Nat Metab | doi: 10.
1038/s42255-021-00357-z
)caused.
This result provides new insights into how alcohol may affect the brain, and is expected to be used to better regulate the effects of alcohol on behavior.
The effects of alcohol on human and mouse behavior (such as motor dysfunction) are thought to be caused by metabolites produced during the breakdown of alcohol.
One of the metabolites is acetate, which is produced by acetaldehyde dehydrogenase 2 (ALDH2), which is abundant in the liver.
Acetate produced by the liver will reach the brain through the bloodstream, where it impairs motor function through the signal transduction of the inhibitory neurotransmitter GABA.
Li Zhang of the National Institute of Alcohol Abuse and Poisoning in Bethesda, Maryland, USA, and colleagues observed this phenomenon in three human brain samples and 11 mice.
ALDH2 is expressed in the astrocytes of the cerebellum-the cerebellum It is the brain area that controls balance and motor coordination.
When ALDH2 was removed from the astrocytes of the cerebellum, the mice did not develop motor dysfunction caused by alcohol intake.
In general, alcohol intake will increase the levels of acetate and GABA in the brain, but removing ALDH2 in astrocytes can prevent this level of increase.
In contrast, removing ALDH2 from the liver failed to affect the levels of acetate or GABA in the brain.
The above research results show that the ability of acetate produced by the brain and liver to affect motor function is different.
The authors concluded that alcohol metabolism may be directly regulated in the brain, and it is expected to discover new targets for altering the effects of alcohol and treat alcohol use disorders.
However, further research is needed to determine whether these mechanisms observed in mice also exist in humans.
ALDH2 in astrocytes selectively regulates acetate produced by alcohol metabolism in cerebellar tissue.
Picture from Zhang et al.
©Nature Nat Metab | doi: 10.
1038/s42255-021-00357-z
