Table 1.
Summary of molecular cascades and involvement categorized by disorder.
| Disorder | Molecular changes affecting redox capacity | Age-related ROS imbalances |
|---|---|---|
| Parkinson’s disease | Parkin mutations, acts on β-catenin degradation | L-type Ca2+ channels in dopamine neurons increase intracellular calcium creating a metabolic stress with production of ROS |
| α-Synuclein mutations, impairs proteasome-mediated proteolysis | ||
| Impaired mitochondrial complex I activity | PINK deficiency causes mitochondrial Ca2+ accumulation with stimulation of ROS production | |
| Reduced GSH activity | ||
| LRRK2 mutations (encodes the Ras/Rho-like GTPase domain) | ||
| Alzheimer’s disease | Reduction in reelin | Disruption in calcium homeostasis associated with increased ROS accumulation and damage |
| Reduced Akt levels in Th neurons | ||
| Accumulation of reelin | p53 conformational alterations due to oxidative stress | |
| Aberrant GSK3β | ||
| Schizophrenia | EPHB1 mutations, acts on GTPase (Ras/Rho) | Age-related reductions in Wnt signaling |
| AKT-1, upregulated in oxidative stress | Increased ROS and extra mitochondrial O2 consumption | |
| Reduction in reelin | ||
| Reduced GSH activity | ||
| Impaired mitochondrial complex I activity |