How do epigenetics regulations affect MDD?

Major depressive disorder (MDD) can be explained as a chronic disease that is neurological
and the pathology cannot be determined exactly. Although it has been suggested that this
disease is caused by genetics, recent studies have found evidence that environmental factors
have an important contribution to the formation of this disease. Epigenetic regulation such as
DNA methylation, histone modification, and microRNA expression, and stress and some
environmental factors can cause MDD.

DNA Methylation

Methylation of the MORC1 gene, which elicits a depression-like phenotype in mice, is a

candidate marker for the development of early-life stress-related MBD in rodents, primates,
and humans undergoing prenatal stress. It has been observed that Proline-Rich Membrane
Anchor 1 (PRIMA1) increases between twelve and fifteen percent in MDD patients compared
to non-patients.

Histone Modifications

Evidence from studies to date supports a role for histone variant H3.3 in the pathogen of
MDD. While H3.3 is activated in depressed human nucleus accumbens (NA) especially in
response to chronic social defeat stress in mice, the use of antidepressant drug inhibits H3.3
dynamics and limits its negative effects.

Noncoding RNAs

Similarly, lncRNAs are similar to non-coding RNAs withsignificant signaling and epigenetic
acts. lncRNAs are extremely expressed in the brain. As a result of their dysregulation shapes
negatively effects some factors like neural stem cell maintenance, neurogenesis and
gliogenesis, HPA axis, neurotransmission, neuroinflammation, neurotrophic factors
expression, stress responses, and neural plasticity. These factors can be accepted as
biomarkers for MDD.

References
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Rojo, S., Quintero, J., & Alvarez De Mon, M. (2022). Nutrition, Epigenetics, and

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https://doi.org/10.3389/fnut.2022.867150

Saavedra, K., Molina-Márquez, A., Saavedra, N., Zambrano, T., & Salazar, L. (2016).

Epigenetic Modifications of Major Depressive Disorder. International Journal of

Molecular Sciences, 17(8), 1279. https://doi.org/10.3390/ijms17081279