e tau protein, which is another marker that accumulates in AD pathology. Overall, it was confirmed that Aβ1-42 aggregation in the hippocampus caused cognitive impairment in AD mice.
The researchers also speculated that ROS-induced mitochondrial damage was linked to neuron survival. To test this idea, they measured the levels of several critical mitochondrial oxidative enzymes, including the anti-aging nicotinamide-nucleotide adenylyltransferase (NMNAT)-3. While NMNAT-3 levels were shown to be lower in AD mice, levels of 3-NT (3-nitrotyrosine), a sign of greater oxidation, increased with age. “With decreased levels of NMNAT-3 and increased levels of 3-NT, it is clear that oxidation promotes mitochondrial dysfunction, which eventually leads to cognitive dysfunction,” Prof. Fukui says.
The researchers are upbeat about the possible ramifications of their findings, particularly in terms of increasing the intake of antioxidant chemicals that can assist our bodies combat ROS. Indeed, many natural antioxidants, such as vitamins E and C, can be obtained from diet. Prof. Fukui finishes by speculating: “Mitochondrial activity and cognitive function may be preserved if mitochondria are protected from ROS. Future study should focus on establishing diagnostic markers to detect early brain changes, as well as investigating substances with high antioxidant activity in mitochondria.”