Abstract Title

BHMT in Multiple Sclerosis Pathology: Remyelination of Axons

Abstract

In demyelinating diseases, such as multiple sclerosis (MS), the loss of myelin disrupts axonal conduction within the central nervous system (CNS), eventually leading to the irreversible deterioration of axons and progression of neurological disability. DNA methylation plays a critical role in regulating gene expression in various neurological pathways, including pathways that drive neurodegeneration in MS. S-adenosylmethionine (SAM), a metabolite in the methionine cycle, is involved in numerous methylation reactions within cells, including on histones and DNA. SAM is downregulated in MS, resulting in decreased gene expression, but can be restored by betaine homocysteine methyltransferase (BHMT) and the BHMT - betaine methylation pathway. Further, studies have shown that DNA methyltransferase 3a (Dnmt3a) is dependent on SAM and is necessary for remyelination. Therefore, the focus of this study was to elucidate the interaction between BHMT and Dnmt3a and provide insight into how BHMT can affect remyelination mechanistically. This study will assist in the investigation of the impact of epigenetic changes and MS pathology.

Modified Abstract

DNA methylation plays a critical role in regulating gene expression in various neurological pathways, including pathways that drive neurodegeneration in multiple sclerosis (MS). S-adenosylmethionine (SAM), a metabolite in the methionine cycle, is involved in numerous methylation reactions within cells, including on histones and DNA. SAM is downregulated in MS, resulting in decreased gene expression, but can be restored by betaine homocysteine methyltransferase (BHMT) and the BHMT - betaine methylation pathway. Further, studies have shown DNA methyltransferase 3a (Dnmt3a) is dependent on SAM and necessary for remyelination. The focus of this study was to elucidate the interaction between BHMT and Dnmt3a providing insight into how BHMT can affect remyelination mechanistically. This study will assist in the investigation of the impact of epigenetic changes and MS pathology.

Research Category

Biomedical Sciences

Author Information

Veronica BousquetFollow

Primary Author's Major

Biology

Mentor #1 Information

Dr. Jennifer

McDonough

Mentor #2 Information

Dr. Ernest

Freeman

Mentor #3 Information

Ms. Sarah

Sternabch

Presentation Format

Poster

Start Date

April 2019

Research Area

Genetic Phenomena | Genetics and Genomics | Molecular Genetics | Nervous System Diseases

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Apr 9th, 1:00 PM

BHMT in Multiple Sclerosis Pathology: Remyelination of Axons

In demyelinating diseases, such as multiple sclerosis (MS), the loss of myelin disrupts axonal conduction within the central nervous system (CNS), eventually leading to the irreversible deterioration of axons and progression of neurological disability. DNA methylation plays a critical role in regulating gene expression in various neurological pathways, including pathways that drive neurodegeneration in MS. S-adenosylmethionine (SAM), a metabolite in the methionine cycle, is involved in numerous methylation reactions within cells, including on histones and DNA. SAM is downregulated in MS, resulting in decreased gene expression, but can be restored by betaine homocysteine methyltransferase (BHMT) and the BHMT - betaine methylation pathway. Further, studies have shown that DNA methyltransferase 3a (Dnmt3a) is dependent on SAM and is necessary for remyelination. Therefore, the focus of this study was to elucidate the interaction between BHMT and Dnmt3a and provide insight into how BHMT can affect remyelination mechanistically. This study will assist in the investigation of the impact of epigenetic changes and MS pathology.