Researcher Information

Abstract

Increased adenosine levels throughout the day promote sleepiness; this chemical is broken down by the enzyme adenosine deaminase (ADA). A single nucleotide polymorphism (SNP) in the ADA gene (rs73598374) has been shown to affect sleep regulation. This ADA SNP substitutes a G allele with an A allele, thus reducing ADA enzymatic activity and resulting in higher adenosine levels. Consistent with the idea that adenosine promotes sleepiness, carriers of the A allele show elevated sleep pressure and increased EEG measures of deep (delta) sleep. Aside from these findings, the extent to which lower ADA enzymatic activity is associated with the homeostatic sleep factor, melatonin, is uncertain. This association is a distinct possibility, however, because adenosine has been shown to increase melatonin production in rat pineal glands. In order to test this possibility, we examined the extent to which the ADA polymorphism is associated with evening melatonin levels, along with several measures of selfreported sleep and mood behaviors. Our findings support the idea that adenosine can enhance melatonin levels. Relative to the GG group (Mean= 19.80, SD =8.61), the AG group (Mean= 27.27, SD = 16.63) had significantly increased melatonin levels, F(1, 83) = 7.27 p=0.008. However, differences in selfreported sleep behavior between the GG group and the AG group were not significant. Interestingly, however, AG carriers reported significantly higher state anxiety (p=0.046) with a trend for increased trait anxiety and moodiness. These findings advanced our understanding of the biochemistry of sleep and uncovered a relationship between ADA gene expression and anxiety.

Faculty Sponsors

Dr. Jaime L. Tartar

Project Type

Event

Location

Alvin Sherman Library

Start Date

4-8-2016 1:00 PM

End Date

4-8-2016 5:30 PM

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Apr 8th, 1:00 PM Apr 8th, 5:30 PM

Adenosine Deaminase Associates with Self-Reported State Anxiety and Evening Melatonin Levels

Alvin Sherman Library

Increased adenosine levels throughout the day promote sleepiness; this chemical is broken down by the enzyme adenosine deaminase (ADA). A single nucleotide polymorphism (SNP) in the ADA gene (rs73598374) has been shown to affect sleep regulation. This ADA SNP substitutes a G allele with an A allele, thus reducing ADA enzymatic activity and resulting in higher adenosine levels. Consistent with the idea that adenosine promotes sleepiness, carriers of the A allele show elevated sleep pressure and increased EEG measures of deep (delta) sleep. Aside from these findings, the extent to which lower ADA enzymatic activity is associated with the homeostatic sleep factor, melatonin, is uncertain. This association is a distinct possibility, however, because adenosine has been shown to increase melatonin production in rat pineal glands. In order to test this possibility, we examined the extent to which the ADA polymorphism is associated with evening melatonin levels, along with several measures of selfreported sleep and mood behaviors. Our findings support the idea that adenosine can enhance melatonin levels. Relative to the GG group (Mean= 19.80, SD =8.61), the AG group (Mean= 27.27, SD = 16.63) had significantly increased melatonin levels, F(1, 83) = 7.27 p=0.008. However, differences in selfreported sleep behavior between the GG group and the AG group were not significant. Interestingly, however, AG carriers reported significantly higher state anxiety (p=0.046) with a trend for increased trait anxiety and moodiness. These findings advanced our understanding of the biochemistry of sleep and uncovered a relationship between ADA gene expression and anxiety.