Each year, some 200,000 people in Germany and 1 million people in Europe suffer a stroke. This happens when blood clots obstruct major vessels and there is no longer sufficient supply of blood to the brain. If doctors manage to break down or mechanically remove the clot, further damage is prevented. Nevertheless, 100 percent of the tissue originally affected and about 70 percent of the cells in adjacent areas die off. Scientists based at the LMU Medical Center, the Charité in Berlin and the University of Maryland, Baltimore (U.S.), led by Dr. Francisco Pan-Montojo (Clinic for Psychiatry and Psychotherapy at University of Munich Hospital) has now been able to demonstrate in several relevant animal models of stroke that glycolic acid can be successfully used to salvage threatened tissue. The experimental treatment imitates a survival strategy of the nematode Caenorhabditis elegans a worm present in the soil, as the researchers report in Advanced Science.

Survival strategies of C. elegans

The nematode C. elegans can withstand even desiccation by entering a special larval stage called dauer. Its metabolism stops as the worm dries— and reactivates again on contact with water. Both situations lead to a stress response with a huge increase in the production of reactive molecules (radicals), increased calcium levels in nerve cells, and functional changes in mitochondria, the energy-generating cell organelles. The fact that C. elegans survives this is substantially due to its ability to increase the production of glycolic acid in its cells upon desiccation, as experimental studies have shown: When glycolic acid production is inhibited, then it dies, whereas externally supplied glycolic acid has a protective effect enabling the worms to survive.

Good protection in animal models

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