Increasing neurogenesis by deleting the Bax gene in mouse models of Alzheimer's improved the animals' performance in tests measuring spatial recognition and contextual memory.
Two different parts to the BAX protein can bind to BH3-only, and these sites function at different stages of BAX activation. When BH3-only binds to one of the regions, BAX becomes able to damage mitochondria.
Lancaster University researchers report a drug developed to treat diabetes shows promise in reversing memory loss associated with Alzheimer's in mouse models of the disease. The drug appears to have a neuroprotective effect, enhancing brain growth factors while reducing amyloid plaques, chronic inflammation and oxidative stress. The drug also slows down the rate of neuron loss.
Researchers report adult neurogenesis not only helps increase the number of cells in a neural network, it also promotes plasticity in the existing network. Additionally, they have identified the role the Bax gene plays in synaptic pruning.
Researchers visualize the molecular changes in a critical cell death protein that force cells to die. Defects in cell death have been linked to the development of diseases such as cancer and neurodegenerative conditions.
