Interplay of oxidative stress and neuroinflammation in alzheimer's: insights into age-driven pathogenesis - PubMed
2 hours ago
- #Alzheimer's disease
- #Neuroinflammation
- #Oxidative stress
- Ageing is the leading risk factor for Alzheimer's disease (AD).
- Oxidative stress, neuroinflammation, and cellular senescence play key roles in AD pathogenesis.
- Mitochondrial dysfunction leads to redox imbalance and excessive ROS production, damaging DNA and promoting amyloid-β accumulation.
- Chronic inflammasome activation in microglia and astrocytes (via NLRP3 and NF-κB) drives neuroinflammation, synaptic loss, and tau pathology.
- Senescent glial and neuronal cells amplify inflammation and oxidative damage via the senescence-associated secretory phenotype (SASP).
- Potential therapies include mitochondria-targeted antioxidants and senolytics, but face challenges like biomarker heterogeneity and antioxidant delivery issues.
- A proposed roadmap suggests monitoring oxidative/inflammatory biomarkers, combinatorial therapies, and personalized interventions to delay AD onset.