Roles of Oxidative Stress in Synaptic Dysfunction and Neuronal Cell Death in Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a brain disorder that progressively undermines memory and thinking skills by affecting the hippocampus and entorhinal cortex. The main histopathological hallmarks of AD are the presence of abnormal protein aggregates (Aβ and tau), synaptic dysfunction, aberrant proteostasis, cytoskeletal abnormalities, altered energy homeostasis, DNA and RNA defects, inflammation, and neuronal cell death. However, oxidative stress or oxidative damage is also evident and commonly overlooked or considered a consequence of the advancement of dementia symptoms. The control or onset of oxidative stress is linked to the activity of the amyloid-β peptide, which may serve as both antioxidant and pro-oxidant molecules. Furthermore, oxidative stress is correlated with oxidative damage to proteins, nucleic acids, and lipids in vulnerable cell populations, which ultimately lead to neuronal death through different molecular mechanisms. By recognizing oxidative stress as an integral feature of AD, alternative therapeutic or preventive interventions are developed and tested as potential or complementary therapies for this devastating neurodegenerative disease.

Trends and hotspots in tea and Alzheimer's disease research from 2014 to 2023: A bibliometric and visual analysis

“…Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the body's antioxidative defenses, plays a recognized and substantial role in the development and progression of AD [ 30 ]. This oxidative stress leads to cellular damage, including harm to neurons and neuronal membranes, thereby contributing to the observed cognitive decline in AD [ 31 ]. Polyphenols encompass a diverse group of compounds that are abundant in tea, particularly in green tea [ 32 ].…”

Uncovering the Early Events Associated with Oligomeric Aβ-Induced Src Activation

“…Oxidative stress is one of the main processes involved in AD pathogenesis [ 36 ]. In former studies, Behl and colleagues demonstrated that Aβ (25–35 and 1–40 peptides) caused increased H 2 O 2 levels and accumulation of lipid peroxides in primary cortical neurons, B12 and PC12 cells, affecting cell metabolism and survival [ 37 ].…”

Preparation, Characterization, Antioxidant Activities, and Determination of Anti-Alzheimer Effects of PLGA-Based DDSs Containing Ferulic Acid

“…In addition, oxidative stress is linked to oxidative damage to proteins, nucleic acids, and lipids in susceptible cell populations, which ultimately results in neuronal death via many molecular processes. The development and testing of alternative therapeutic or preventive measures as possible or supplementary therapies for this debilitating neurodegenerative disease is enabled by the recognition of oxidative stress as a key component of AD. − …”

“…The development and testing of alternative therapeutic or preventive measures as possible or supplementary therapies for this debilitating neurodegenerative disease is enabled by the recognition of oxidative stress as a key component of AD. 27 − 29 …”