Table 1.

Protective effects of neuroactive steroids on Aβ-induced mitochondrial impairment.

DHEA	Allopregnanolone	E2
In vitro Forebrain mitochondria from male Swiss mouse + Aβ1–42 (4 µM) or Aβ25–35 (50 µM) for 20 min   DHEA (3, 10 or 30 µM, 20 min) ↓ mitochondrial respiration dysfunction through σ1 receptor mechanism ↓ increased ROS production [108]	In vitro PC12 cells + aggregated Aβ25–35 (20 µM, 24 h)   Allopregnanolone pretreatment (10 µM, 2 h) ↓ ROS generation ↓ SOD activity [109]	In vitro Choroid plexus explants or cell line Z310 + Aβ1–42 (0.66 µM, 24 h)   E2 pretreatment (1 µM, 8–12 h)↓ ROS production, ↓ Aβ uptake [110]   In vivo Ovariectomized 3xTg-AD mice   E2 treatment (0.25 mg continuous 90-day pellet) prevented in isolated forebrain mitochondria: ↓ respiration, ↓ energy deficits ↓ Aβ load, ↓ lipid peroxidation [107]

↓: decrease ↑: increase vs. Aβ condition.