Neurology Central

Traumatic CNS injury and the inflammatory stem cell niche: an interview with Aileen Anderson


Aileen Anderson is a Professor at the University of California Irvine (CA, USA) and is also the Director of the Sue & Bill Gross Stem Cell Research Center at the institution.

In this interview, Aileen speaks to us about her talk at the 21st Spinal Research Annual Network Meeting (6–7 September 2019, London, UK) on traumatic CNS injury and the inflammatory stem cell niche. Aileen also discusses the obstacles involved with tissue regeneration following injury and the techniques she employs to help overcome the challenges with strong inflammatory responses.

1.What inspired you to work in the field of stem cells in relation to spinal cord injuries?

When I first started up my own lab, which focused on spinal cord injuries, I was really interested in the intersection between how the immune system might be communicating to the CNS and what role that might play in terms of either damage or recovery of function. Thus, I employed a number of spinal cord injury models in mice and at the time, there weren’t very many people who were manipulating mice in this way.

I was approached by collaborators who had isolated neural stem cells and they really wanted to transplant these cells and look at what happened following a spinal cord injury (i.e., whether they could have a therapeutic benefit). There weren’t many labs that were working on immunodeficient mice at all and our collaborators were particularly keen to look at the potential of those cells and the absence of immunorejection, so it was a match right from there.

This happened in the early 2000s and human neural stem cells had only really been revealed to be present in an adult niche in 1998, so it was early in the game of stem cells and regenerative medicine. It was easy to see that the potential of this field was going to be big.

2.You’ve presented a talk on ‘Traumatic CNS injury and the inflammatory stem cell niche’ – could you provide us with an overview of this?

My talk was the culmination of a lot of work that has originally come out of those very translational projects that we did in my lab. When you go to clinical trial, or think about going to clinical trial, there are a lot of elements you have to know – that is, nitty gritty details that we would never think about asking when doing basic science research. For example, the dose of cells, timing of transplantation and all the variables that you would use to define a clinical trial.

Along the way of doing those translational studies, we made some observations that were surprising to us. One of them was that if we looked at timing and transplanted a multipotent human neural stem cell population super early and acutely after injury, those cells all got recruited into the epicenter. Additionally, these cells like to make astrocytes and we didn’t see functional recovery.

In contrast, if we delayed transplantation to weeks or months after injury, those cells didn’t exhibit the same characteristics – where they went and what they did was different. They migrated away from the injury and didn’t get trapped into making astrocytes. We saw many more oligodendrocytes and neurons and we did see functional recovery. Thus, this raises the question as to why does that happen? It was obvious that there had to be cues in the microenvironment that those cells were listening to.

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