There is still a lot to learn about the causes of depression.
Karmel Choi, clinical psychologist and assistant professor of psychology at the Harvard Medical School, takes a look inside our genes for clues.
Karmel Choi is a Clinical Psychologist, Director of the Precision Prevention Program in the Center for Precision Psychiatry at Massachusetts General Hospital, and Assistant Professor at Harvard Medical School. Her group uses methods from data science, epidemiology, and statistical genetics to understand the development of depression across the life course and identify actionable strategies for prevention. She serves as the outreach representative for the Psychiatric Genomics Consortium’s Major Depressive Disorder Working Group, which seeks to discover how genetic factors contribute to depression.
Linking Genes to Depression
Depression is a common condition and one of the leading causes of disability worldwide, affecting more than one in five people in their lifetime. While it’s been clear for some time that genetics contribute to depression, the exact genes and biological processes involved have remained largely unknown.
To address this gap, researchers from 29 countries conducted the largest genetic study of depression to date. We analyzed anonymized genetic data from over five million people, both with and without depression. This was the first study of its kind to include participants from many different ancestry backgrounds, making the findings more globally relevant.
We identified 697 genetic variants—specific places along the genome—that were linked to depression. Nearly 300 of these were previously unknown. Each variant contributes a small increase to the risk of depression, but together, their effects add up. By incorporating new knowledge about these variants, we improved on our ability to predict an individual’s depression risk.
We also mapped these genetic variants to biological pathways. We found key roles for neurons—brain cells that send and receive signals—as well as brain regions involved in regulating emotions, like the amygdala, hippocampus, and thalamus. We also identified processes like calcium signaling and endocytosis that may influence how neurons function in depression.
Interestingly, some of the identified genes overlap with those targeted by existing drugs not only for depression, but also sleep disorders and pain. This opens the door to refining current treatments and repurposing existing medications to more effectively treat depression.
This study underscores the strong biological basis of depression and highlights the value of large, collaborative genetics research in advancing personalized and effective treatments.
Read More:
[Cell] – Trans-ancestry genome-wide study of depression identifies 697 associations implicating cell types and pharmacotherapies
Psychiatric Genomics Consortium
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