Investigating the Effects of Antide Treatment on the Preventative and Restorative Effects of Hippocampal Damage in Alzheimer’s Disease Rats

After menopause women are more likely to develop Alzheimer’s disease (AD) than men. This predisposition is due to the drop in estrogens (E) that occurs following menopause. This drop in neuroprotective estrogens is accompanied by a rise in luteinizing hormone (LH). Elevated LH has been associated with decreased performance on cognitive tasks as well as loss of memory, and the development of AD. Prior work in the Thornton Lab has utilized Antide, a GnRH antagonist, to decrease the production of LH in an AD rat model. By infusing small doses of neurotoxins Beta-Amyloid and ibotenic acid into the dorsal hippocampus, a brain region critical for learning and memory, we are able to produce a rat model, displaying early stages of AD. We are presently testing whether lowering LH with Antide can decrease cognitive defects and/or damage to neurons when administered either prior to or following neurotoxin infusion. We will use immunocytochemistry for NeuN, a marker for neurons, to examine the number of neurons in animals that received Antide treatment just before or following neurotoxin infusion to investigate the potential for preventative as well as restorative effects of Antide treatment on memory and cell death associated with AD. Although E has neuroprotective effects, E replacement therapies heighten the risks of ovarian, breast, and other forms of cancer. If targeting LH effectively reduces the neuronal damage associated with AD, this could introduce a safer way to treat post-menopausal women in either a preventative or restorative manner to combat early signs of AD