Description
The activation of repair mechanisms with therapeutic compounds is an active area of research that has recently been focused on slowing the processes linked to neural aging. Previous studies targeted on Alzheimer’s disease have largely focused on altering amyloid beta production or MAP-Tau phosphorylation profiles. As to date this targeted approach has met with limited success. New methods for the treatment or preventions of neural degenerative disorders are underway and have revitalized the concept of hormesis, where low doses of an otherwise toxic compound can exhibit neural protective properties. The aims of these studies were to more fully examine the impact of the neural protective compound, J147 for its ability to mitigate the acute and long-term effects of traumatic brain injury. In addition, we examined nicotine, a compound that humans often have common exposure. Interacting via acetylcholine receptors, low dosages of nicotine are known to attenuate anti- inflammatory responses. We demonstrate that J147 and nicotine treatment can improve the outcome of flies exposed to mild trauma, in part through altering the molecular pathways associated with inflammation within the adult Drosophila central nervous system.
