| Abstract |
In Alzheimer’s disease (AD) and multiple sclerosis (MS) histone methylation is severely reduced. This hypomethylation leads to aberrant gene expression that brings about disease-causing plaque and lesion buildup within the central nervous system. It is known that this aberrant gene expression affects mitochondria in these diseases. I hypothesized that introducing methyl donors could prevent hypomethylation of histone H3, as well as dysfunction of mitochondria in mouse models of AD and MS. I tested the effects of the methyl donor betaine (also known as trimethylglycine). We administered betaine in drinking water to the APP/PS1 mouse model of AD, and the Cuprizone mouse model of MS for four weeks. The aim of this study was to measure the protective effects of the methyl donor betaine on mitochondrial complexes downregulated in neurodegenerative diseases. Protein was isolated from the brains of mice with and without betaine. The levels of different mitochondrial complex genes in the presence and absence of betaine were measured using Western blotting, JC1 staining, immunohistochemistry (IHC), and densitometry. This research has important implications for developing new therapies to treat AD and MS.
|
| Modified Abstract |
In Alzheimer’s disease (AD) and multiple sclerosis (MS) histone methylation is severely reduced. This hypomethylation leads to aberrant gene expression that brings about disease-causing plaque and lesion buildup within the central nervous system. We administered betaine in drinking water to the APP/PS1 mouse model of AD, and the Cuprizone mouse model of MS to measure its effects on repairing mitochondria. This research has important implications for developing new therapies to treat AD and MS.
|
