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Related Experiment Video

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Animal Models of Depression - Chronic Despair Model (CDM)

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Published on: September 23, 2021

Polymorphisms in melatonin synthesis pathways: possible influences on depression.

Daniel F Kripke¹, Caroline M Nievergelt, Greg J Tranah

¹Department of Psychiatry, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093, USA. dkripke@ucsd.edu.

Journal of Circadian Rhythms

|August 11, 2011

Summary

The ASMT gene

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Area of Science:

Neuroscience
Genetics
Psychiatry

Background:

The acetylserotonin methyltransferase (ASMT) gene's single nucleotide polymorphism (SNP), rs4446909, affects ASMT enzyme expression and melatonin synthesis.
The G allele of rs4446909 is linked to reduced ASMT activity and has been associated with depressive disorders.
ASMT and arylalkylamine N-acetyltransferase (AANAT) gene variations may influence mood regulation through N-acetylserotonin and melatonin pathways.

Purpose of the Study:

To investigate the association between the rs4446909 polymorphism and mood disorders.
To replicate previous findings linking ASMT activity to depression and explore its potential role in bipolar disorder relapse.
To examine the relationship between AANAT gene polymorphisms and depression.

Main Methods:

Genotyping of rs4446909 in four distinct research cohorts, including patients with delayed sleep phase disorder and control groups.
Utilizing an Illumina Golden Gate assay to survey 610 SNPs.
Assessing depressive symptoms via self-report scales and evaluating lithium treatment response in bipolar patients.

Main Results:

A significant association was found between rs4446909 and depressive symptoms in individuals with delayed sleep phase disorder (P = 0.01).
No significant associations were observed in other study groups, including a sleep clinic patient cohort, elderly cohorts, or in relation to bipolar disorder treatment response.
Two AANAT SNPs showed no association with depression.

Conclusions:

The study did not find strong evidence for rs4446909 significantly influencing mood, though a partial replication suggests a possible modest effect.
Larger sample sizes and improved phenotyping in younger populations may yield more conclusive results.
The findings do not strongly support rs4446909 as a major genetic factor in mood disorders but warrant further investigation.