The fellow, Diego Gómez-Nicola, from the CNS Inflammation group at the University of Southampton in the United Kingdom, examined how a specific cell protein receptor called CSF1R controls the spread and inflammation in neurodegenerative diseases.

As part of the European Union (EU)-funded Marie Curie project called PRONEURODEG, Gómez-Nicola discovered that a laboratory drug targeting the identified protein could help effectively combat the disease. The results, based on research with mice, could open new avenues for the regulation of Alzheimer-like reactions in the brain related to the loss of memory and other mental abilities.
The researcher studied the biology of microglial cells, which play a leading role in the development and maintenance of the inflammatory reaction, and how they increased in number during different neurodegenerative conditions.

“By targeting the CSF1R receptor with a selective inhibitor, I was able to delay the symptoms of the disease and also prevent the loss of neurons,” says Gómez-Nicola. ”We selectively targeted the CSF1R with a small-molecule inhibitor delivered systemically, which slowed the onset of the clinical and pathological course of prion disease, and extended the survival rate,” explains the researcher.
Gómez-Nicola’s work also looked at neural stem cells, the intrinsic self-repair mechanism in adults. He found that some activity during the disease compensated for cell death at the hippocampus, the brain structure involved in learning and memory. “We showed that a self-repair mechanism is in place during widespread neurodegeneration, leading to new avenues for treatment,” affirms Gómez-Nicola.

PRONEURODEG project coordinator, Hugh Perry, and also Professor of Experimental Neuropathology at the University of Southampton, says the research looked at an aspect that all neurodegenerative diseases have in common: the activation of immune cells and their increase in number. “[The researchers] know that infections elsewhere in the body communicate with the brain, and that is why we feel ill. However, sometimes this response and the increase of immune cells become harmful,” he says.

Gómez-Nicola tested on mice – and analysed the results – to show how self-repair might work with humans. “Diego found that the increase in brain immune cells was a result of local proliferation. He showed that if we are able to block this proliferation, then the mice could live longer. This indicates how the immune system is involved: the immune cells are making it worse,” adds Perry. For humans, the results mean that harmful immune responses could be controlled by managing the CSF1R receptor.

In the words of Gómez-Nicola “the Marie Curie grant not only supported the research work, but it also helped me personally progress to the next step of my career: establishing my own independent research group.”