Redox changes and cellular senescence in Alzheimer's disease

Area of Science:

• Neuroscience
• Cellular Biology
• Biochemistry

Background:

• Alzheimer's disease (AD) pathogenesis involves complex cellular mechanisms.
• Redox processes and cellular senescence are implicated in neurodegenerative disorders.
• Dysregulation of reactive oxygen species (ROS), heme metabolism, and mitochondrial function are key factors.

Approach:

• This review examines the interplay between redox imbalance, cellular senescence, and AD.
• It explores how disruptions in heme metabolism and mitochondrial function exacerbate these processes.
• The review synthesizes current understanding of these molecular mechanisms in AD.

Key Points:

• Elevated ROS, stemming from beta-amyloid, tau, and heme dyshomeostasis, damages cellular components and impairs neuronal function.
• Oxidative stress can trigger cellular senescence and the senescence-associated secretory phenotype, promoting inflammation.
• Mitochondrial dysfunction and endoplasmic reticulum stress further aggravate ROS production and cellular damage.

Conclusions:

• Changes in redox state and cellular senescence are critical contributors to AD.
• Perturbations in heme metabolism and mitochondrial function significantly impact these pathways.
• Further research is needed to develop effective therapeutic strategies targeting these mechanisms for clinical application.