The Role of Oxidative Stress and DNA Epigenetic on Aβ Plaque Accumulation in Alzheimer’s Disease

Lauren Sauer 

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that results in memory loss and eventually death. In the past, the central cause of AD was attributed to the accumulation of the amyloid beta (Aβ) protein in the central nervous system. More recently, the pathogenic pathway of AD has expanded to include oxidative stress and epigenetic modifications. This review focuses on the main components of Alzheimer’s disease and suggests a potential explanation for the disease’s mechanism. Recent research indicates that AD patients have increased transcription levels of amyloid-β precursor protein and b-site amyloid- β precursor protein-cleaving enzyme 1, caused by histone hyperacetylation and DNA demethylation. Furthermore, oxidative stress may be responsible for the altered levels of DNA methylation and histone acetylation. Ultimately, epigenetic modifications leads to Aβ and neurofibrillary tangle accumulation in Alzheimer’s patients.

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