Although no one is announcing a cure for Alzheimer’s disease just yet, research recently conducted at the University of Southern California does at least offer a glimmer of hope. Using drugs known as TSPO (translocator protein) ligands, scientists there have successfully halted and even reversed the effects of Alzheimer’s in mice.

The mice, all of which were male, had been genetically engineered to develop the disease. The drugs were tested on both 7-month-old young adult mice and 24-month-old elderly mice. Because the TSPO ligands increase production of steroid hormones, it was important that the animals’ existing testosterone levels be kept low before beginning the treatment. While this had already occurred naturally with the older mice as a result of aging, the younger ones had to be castrated in order to bring their levels down.

After receiving once-a-week treatments for four weeks, all of the mice showed improvements. This was particularly noteworthy with the older mice, as their Alzheimer’s had become quite severe. After the four treatments, however, they showed “significant lowering of Alzheimer’s-related pathology and improvements in memory behavior.”

It’s already known that TSPO ligands help protect nerve cells by reducing inflammation, and that they increase the production of neuroactive hormones in the brain. The scientists now plan on determining which factor plays more of a part in the success with the mice, then developing new TSPO ligands designed around those findings.

“From the optimistic perspective, our data provide very promising findings with tangible potential benefits for both the prevention and treatment of Alzheimer’s,” said lead scientist Prof. Christian Pike. “On the pessimistic side, research scientists have developed many interventions that cured Alzheimer’s in mice but have failed to show significant benefits in humans. A critical direction we are currently pursuing is successfully translating these findings into humans.”

A paper on the research was recently published in The Journal of Neuroscience.

Source: University of Southern California