Naltrexone as a therapeutic for the treatment of Alzheimer's Disease
Potential treatment via hormone modulation of beta amyloid production
A risk factor for Alzheimer's disease (AD) is increased blood levels of gonadotropins, particularly Luteinizing Hormone (LH). Professor Martins and his group has identified that LH plays a role in AD pathogeneisis, particularly in regulating beta amyloid (Aß). The use of LH lowering agents such as leuprolide has been shown to lower A accumulation in the brains of transgenic mice and improve cognition, indicating that lowering LH levels is a target for developing therapeutic strategies.
Already affecting an estimated 20 million people worldwide, the prevalence of this debilitating disease is expected to double by 2025 due to the ageing population. The market for treatments that ease the symptoms of the disease reached nearly US$3 billion in 2004; however there are presently no disease modifying drugs available.
Naltrexone is currently approved on the pharmaceutical benefits scheme for the management of alcohol and opioid dependence. Work by ECU's Professor Ralph Martins and collaborator, Professor Gary Hulse (UWA) has identified that this compound can lower LH levels in blood. The group now have preliminary data showing a trend towards a reduction in Aß levels in patients following Naltrexone treatment. In addition, the group has identified another feature of Naltrexone in that it can reduce A mediated toxicity in neuronal cell culture, suggesting that it can prevent A-induced neuronal death. A provisional patent has been filed for Naltrexone as a therapeutic for the treatment of AD.