Table 3.
Factors predisposing patients to dementia following cancer therapy.
| Possible Mechanism/Function | ||
|---|---|---|
| Genetic factors | APOE-4 | Blood brain barrier dysfunction, oxidative stress, and inflammation |
| IL-1R1 | Inflammation | |
| COMT | Neurotransmitter metabolism | |
| BDNF | Mediation of neuroplasticity | |
| BIN1 | tau pathology | |
| TOMM40 | α-synuclein accumulation, oxidative damage, mitochondrial dysfunction and neuroinflammation | |
| OPRM1 | Activation of the mu-receptor | |
| Morbidity | Stroke | Brain atrophy/brain damage |
| Diabetes | Induction of vascular damage | |
| Biomarkers | pNF-H | Serum marker of axonal damage |
| TNF-α, sTNFRI/II | Inflammatory cytokine and receptor | |
| IL-1β, IL-2, IL-10, IL-6, IL-8 | Alteration of blood brain barrier | |
| NAA/Cho, NAA/mI | Neurological markers |
APOE, apolipoprotein E; BDNF, brain-derived neurotrophic factor; COMT, catechol-O-methyltransferase; IL1-R1, interleukin-1-receptor1; BIN1, bridging integrator 1; OPRM1, mu opioid receptor gene; pNF-H, phosphorylated neurofilament heavy subunit; TNF-a, tumor necrosis factor-alpha; sTNFRI/II, tumor necrosis factor-receptor type I/II; Cho, choline; mI, myo-inositol; NAA, N-acetylaspartate; TOMM40, translocase of outer mitochondrial membrane 40.