Scientists, using "gene therapy" to increase the levels of a single enzyme, recently created a strain of mice with increased physical abilities.
Aged mice, with increased GluN2B subunit expression, exhibited improved long-term spatial memory, comparable to young mice.
Total femur bone volume, length, cross-sectional volume, and cortical volume and thickness were increased in mice with increased body mass, independent of rAAV treatment.
In addition, hippocampal slices from aged mice with increased GluN2B subunit expression exhibited enhanced NMDA receptor-mediated excitatory post-synaptic potentials (EPSP).
Interestingly, T-0681 treated mice with increased ABCG5/G8 expression exhibited the same characteristics.
Some mutant mice with increased hippocampal plasticity show enhanced learning [58] while others exhibit learning deficits [59], [60], [61].
Speakman et al. [12] elegantly demonstrated that mice with increased respiratory rates and reduced energetic conversion efficiency due to spontaneously uncoupled mitochondria lived longer than their counterparts.
Western blot analysis of the serum (Methods S2) showed six major bands recognized by the serum of Ae. aegypti-exposed mice, with increased reactivity observed in mice exposed four times to mosquito feeding (Fig. 2A).
Taken together, the data indicate that phosphorylated p38 MAPK levels increase in association with ROS in hyperglycemic mice with increased oxidative stress and return to wildtype levels in SOD2-STZ mice that have reduced superoxide load despite hyperglycemia.
However, a variety of human α-synuclein transgenic mice with increased α-synuclein aggregation, motoric dysfunction, and neurodegeneration have failed to show overt neurodegeneration of dopaminergic neurons [10], [11], [12].
