Oxidative Stress and Neuroinflammation in Alzheimer’s Disease: Molecular Mechanisms and Therapeutic

Dear Colleagues,

Alzheimer’s disease (AD) is driven by tightly interconnected mechanisms involving oxidative stress, chronic neuroinflammation, and progressive neuronal degeneration. Oxidative imbalance not only accelerates amyloid-beta and tau pathology but also amplifies neuroimmune activation, mitochondrial dysfunction, and redox-sensitive signaling pathways. Importantly, accumulating evidence shows that these oxidative and inflammatory disturbances contribute to the activation of regulated cell death programs—such as apoptosis, necroptosis, and ferroptosis—which further promote neuronal loss and disease progression. These cell death pathways do not act in isolation; rather, they operate as critical downstream consequences of sustained redox dysregulation and inflammatory stress.

This Special Issue, “Oxidative Stress and Neuroinflammation in Alzheimer’s Disease: Molecular Mechanisms and Therapeutic,” aims to highlight emerging insights into how oxidative stress, immune activation, and cell death mechanisms converge to shape AD pathophysiology. We welcome original research and review articles that elucidate molecular redox regulation, neuroimmune crosstalk, mitochondrial function, and antioxidant-based therapeutic strategies. Studies characterizing how oxidative stress modulates specific cell death pathways—and how antioxidants may mitigate these processes—are also encouraged.

By integrating multidisciplinary perspectives across neuroscience, immunology, and redox biology, this Special Issue seeks to deepen our mechanistic understanding of AD and support the development of innovative antioxidant-based interventions targeting neuroinflammation and cell death. We look forward to your valuable contributions.

Dr. Seung-Hoon Yang
Guest Editor

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