Potential treatment could prevent brain damage in premature babies

A Swedish study reports a potential treatment to prevent premature baby brain damage, using a new prenatal brain model.

Researchers observed how cerebral haemorrhages (bleeding in the brain) affect stem cells during preterm birth and successfully tested an antidote that reduced the damage.

They identified how neural stem cells in preterm infants are harmed when blood enters the brain.

When red blood cells seep into the subventricular zone and break down, levels of interleukin-1 (IL-1) – an inflammatory protein – rise, causing stem cells to stop functioning properly.

Professor Anna Herland, senior lecturer at the AIMES research centre at KTH Royal Institute of Technology and Karolinska Institutet, explained: “Instead of remaining flexible and ready to grow into different types of brain cells, the stem cells start changing too early or stop growing altogether.”

Intraventricular haemorrhage is a frequent and severe complication of preterm birth.

When red blood cells enter the brain, they rupture and release inflammation-triggering components like haemoglobin, which triggers pro-inflammatory proteins linked to immune response.

“Blood and its degradation products cause a strong inflammatory response in brain support cells, glia cells, that are meant to protect and nourish the brain and repair damage,” Herland said.

The model developed by the Swedish team enables these effects to be studied in a system that closely mimics human brain mechanisms.

Working with researchers at Ege University in Turkey and Harvard University in the US, the team built the model using lab-grown human brain cells derived from stem cells.

This platform was then used to test an IL-1 antagonist – a drug that blocks IL-1 activity. The treatment suppressed interleukin-1 levels and provided partial protection to the stem cells.

The team also examined cerebrospinal fluid from patients with haemorrhage.

This showed a clear but less intense effect on neural stem cells, consistent with lower concentrations of toxic breakdown products and the fluid’s growth factors, nutrients and anti-inflammatory proteins.

“This is one of the most complex in vitro models I have constructed and seen,” Herland said.

“That we could recapitulate all these interactions is amazing.

“That we can then see relevant responses to both simulated conditions and patients’ samples is really important, as there is currently no established treatment for these patients.”

The team plans to use the platform to study different levels of injury and scale up the model.

“We hope to screen more treatments that could be even more effective than the one we studied,” Herland added.