'Plaques' of amyloid beta (Ab) and tau protein 'tangles' develop in the brain during Alzheimer's Disease, leading to the death of brain cells and disruption of chemical signaling between neurons.

Using gene therapy techniques, Pedro Chacon and Alfredo Rodrguez-Tobar augmented the amount of Hes1 in cultured neurons. Increasing the amount of Hes1, directly or by activating the protein NF-kB (which in turn up-regulate the cell's own Hes1), abolished the effect of Ab and prevented neuron death. Additionally another growth factor, TGFb, which can also activate NF-kB, was able to prevent the effects of Ab on neurons by improving levels of Hes1.
Pedro Chacon explained, "Ab usually decreases the length of dendrites and GABAergic connectivity of neurons, however these effects were completely reversed by Hes1, NF-kB, and TGFb. When we grew neurons in a concentration of Ab which normally kills most cells, 50% of the neurons with extra Hes1 were able to survive."
These results demonstrate that neurons can be protected from the effects of Ab by increasing the amount of Hes1 in the cells. By clarifying the roles of NGF or TGFb in Hes1 protection this research provides strategies for limiting the effects of Alzheimer's disease.
Source-Eurekalert