Functional ADA Polymorphism Increases Sleep Depth and Reduces Vigilant Attention in Humans

Jul 8, 2011Cerebral cortex (New York, N.Y. : 1991)

A common genetic variation linked to deeper sleep and lower alertness in people

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Abstract

The nonsynonymous c.22G>A polymorphism (rs73598374) of adenosine deaminase is associated with elevated sleep pressure and poorer cognitive performance.

Carriers of the G/A genotype (n = 29) performed worse on attention tasks compared to G/G homozygotes (n = 191).
Deep sleep and slow-wave oscillations in non-REM sleep were significantly higher in G/A genotype individuals.
Attention and vigor were reduced in G/A carriers, while measures of sleepiness, fatigue, and saliva α-amylase levels were increased.
The findings suggest that reduced adenosine deaminase activity may impact both sleep quality and cognitive functions.

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Homeostatically regulated slow-wave oscillations in non-rapid eye movement (REM) sleep may reflect synaptic changes across the sleep-wake continuum and the restorative function of sleep. The nonsynonymous c.22G>A polymorphism (rs73598374) of adenosine deaminase (ADA) reduces the conversion of adenosine to inosine and predicts baseline differences in sleep slow-wave oscillations. We hypothesized that this polymorphism affects cognitive functions, and investigated whether it modulates electroencephalogram (EEG), behavioral, subjective, and biochemical responses to sleep deprivation. Attention, learning, memory, and executive functioning were quantified in healthy adults. Right-handed carriers of the variant allele (G/A genotype, n = 29) performed worse on the d2 attention task than G/G homozygotes (n = 191). To test whether this difference reflects elevated homeostatic sleep pressure, sleep and sleep EEG before and after sleep deprivation were studied in 2 prospectively matched groups of G/A and G/G genotype subjects. Deep sleep and EEG 0.75- to 1.5-Hz oscillations in non-REM sleep were significantly higher in G/A than in G/G genotype. Moreover, attention and vigor were reduced, whereas waking EEG alpha activity (8.5-12 Hz), sleepiness, fatigue, and α-amylase in saliva were enhanced. These convergent data demonstrate that genetic reduction of ADA activity elevates sleep pressure and plays a key role in sleep and waking quality in humans.

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Functional ADA Polymorphism Increases Sleep Depth and Reduces Vigilant Attention in Humans

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