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Optimized Analysis of DNA Methylation and Gene Expression from Small, Anatomically-defined Areas of the Brain
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Increased DNA methylation in the parvalbumin gene promoter is associated with methamphetamine dependence

Siriluk Veerasakul1,2, Paritat Watiktinkorn3, Samur Thanoi1,2

  • 1Department of Anatomy, Faculty of Medical Science, Naresuan University, Phitsanulok, 65000, Thailand.

Pharmacogenomics
|August 25, 2017
PubMed
Abstract

Insights

Methamphetamine (METH) dependence and psychosis are linked to increased DNA methylation of the PVALB gene promoter. This epigenetic change may explain GABAergic deficits in METH users.

Area of Science:

  • Neuroscience
  • Epigenetics
  • Psychiatry

Background:

  • Parvalbumin (PV)-containing GABAergic neurons are crucial for brain function and are implicated in schizophrenia and psychosis models.
  • Methamphetamine (METH) administration affects these neurons, suggesting a role for epigenetic mechanisms.

Purpose of the Study:

  • To investigate the association between METH dependence, METH-induced psychosis, and DNA methylation of the PVALB gene promoter.
  • To explore potential epigenetic alterations contributing to GABAergic deficits in METH users.

Main Methods:

  • Pyrosequencing was used to measure PVALB promoter methylation in 100 METH-dependent individuals and 102 controls.
  • Global DNA methylation was assessed using long interspersed nucleotide element-1 (LINE-1) methylation as a reference.

Main Results:

  • A significant elevation in PVALB promoter methylation was found in individuals with METH dependence and METH-induced psychosis.
  • No significant changes in LINE-1 methylation were observed, indicating a specific effect on the PVALB promoter.

Conclusions:

  • Elevated PVALB methylation is specifically associated with METH-induced psychosis.
  • This epigenetic modification may underlie the observed GABAergic deficits in METH dependence.
Keywords:
DNA methylationmethamphetamine dependenceparvalbumin

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