The Role of Oxidative Stress-Induced Epigenetic Alterations in Amyloid-βProduction in Alzheimer’s Disease

Abstract

An increasing number of studies have proposed a strong correlation between reactive oxygen species (ROS)-induced oxidative stress (OS) and the pathogenesis of Alzheimer's disease (AD). With over five million people diagnosed in the United States alone, AD is the most common type of dementia worldwide. AD includes progressive neurodegeneration, followed by memory loss and reduced cognitive ability. Characterized by the formation of amyloid-beta (Aβ) plaques as a hallmark, the connection between ROS and AD is compelling. Analyzing the ROS response of essential proteins in the amyloidogenic pathway, such as amyloid-beta precursor protein (APP) and beta-secretase (BACE1), along with influential signaling programs of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and c-Jun N-terminal kinase (JNK), has helped visualize the path between OS and Aβ overproduction. In this review, attention will be paid to significant advances in the area of OS, epigenetics, and their influence on Aβ plaque assembly. Additionally, we aim to discuss available treatment options for AD that include antioxidant supplements, Asian traditional medicines, metal-protein-attenuating compounds, and histone modifying inhibitors.

Neuroprotective Effects of Biochanin A against β-Amyloid-Induced Neurotoxicity in PC12 Cells via a Mitochondrial-Dependent Apoptosis Pathway

“…Several recent review studies have reported that extracellular Aβ causes oxidative stress to the mitochondria, which thus leads to its inevitable dysfunction [11,12]. Additionally, in vivo studies have also reported that Aβ is highly linked to mitochondrial structural abnormalities, as it was found to accumulate within mitochondria in the brains of AD patients [13,14].…”

Sevoflurane postconditioning protects the myocardium against ischemia/reperfusion injury via activation of the JAK2–STAT3 pathway

“…Reactive oxygen species are involved in many diseases, including neurological diseases (Zuo et al, 2015b), heart failure (Zuo et al, 2015a) and hypertension (Zuo et al, 2014b). A large number of studies have shown that ischemic postconditioning can significantly reduce ROS production, thereby reducing myocardial I/R injury (Barsukevich et al, 2015; Singh et al, 2012; Zhao et al, 2003).…”

The role of the Wnt canonical signaling in neurodegenerative diseases

“…Aβ accumulation in the brain and in cerebral blood vessels causes neurotoxicity by directly inducing oxidative stress [79] and by indirectly promoting microglia activation [80]. Aβ accumulation in blood vessels can impair also the blood-brain barrier (BBB) [81], exacerbating the disease progression.…”