高頻度の飲酒は、アルコール使用障害のある人のシナプス密度低下と相関する

Chronic alcohol use leads to synaptic dysfunction in preclinical studies. However, whether in vivo synaptic density deficits are found in people with alcohol use disorder (AUD) remains unclear.

Thirty-two people with AUD (17 women) and 29 controls (17 women) completed one positron emission tomography (PET) brain imaging scan with the radiotracer [11C]UCB-J, which binds to SV2A, a marker of synaptic density. Levels of synaptic density were quantified by estimating binding potential (BPND) across four regions of interest: frontal cortex, striatum, hippocampus, and cerebellum.

People with AUD were on average(±SD) 43±13 years old and most met criteria for mild or moderate AUD. Controls were 37±12 years old. People with AUD had on average 11% lower [11C]UCB-J BPND than controls in the frontal cortex (F(1,62)=13.074, p<0.001), striatum (F(1,60)=10.283, p=0.002), hippocampus (F(1,60)=5.964, p=0.018), and trending in the same direction in cerebellum (F(1,50)=3.438, p=0.070). Among people with AUD, lower [11C]UCB-J BPND was significantly related to more drinks per drinking day in the frontal cortex (p=0.022) and striatum (p=0.026). People with AUD performed worse on executive function than controls (p=0.020), but this was not related to [11C]UCB-J BPND.

Synaptic density deficits are evident, even in people with mild-to-moderate AUD, with greater deficits in those with greater drinking severity. These findings underscore the potential of synaptic restoration as a therapeutic target for AUD.

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This work was supported by the National Institute of Health.