Aging hinders the retina’s ability to regenerate neurons

The Levi Todd Laboratory is not studying ways to prevent neuron death, but rather the possibilities for restoring the nervous system after neuron loss. The basis of this strategy is the use of glia, cells that support and nourish neurons in the brain and retina. In some animals, such as zebrafish and frogs, glia naturally sense neuron loss and transition to a state similar to that of stem cells in order to carry out replacement. In the last decade, experts have learned to trigger a similar process in the retina of young mice. However, until now, almost nothing has been studied about how well such approaches work in aging tissues, even though age‑related degenerative diseases constitute the main problem for medicine.

In the study, the team applied several regeneration strategies based on transcription factors and found that the efficiency of glia transforming into neurons заметно declines with age. According to Todd, there are two main reasons for this. The first is fundamental: the neurons and glia that a person is born with remain with them for life, unlike skin or liver cells, which are constantly renewed. Over time, these cells become fatigued and lose the plasticity that is characteristic of a young nervous system. The second reason is related to the so-called “inflammaging” — the age‑related intensification of inflammatory processes. With age, the barrier between the circulatory system and the brain (the blood‑brain barrier) weakens, and this exacerbates problems with tissue repair.

At the same time, researchers have found a potential way to partially overcome this barrier. The use of anti‑inflammatory steroids has partially restored the regenerative response of the retina in older animals.Perhaps regeneration in the aging nervous system can be enhanced, although the task becomes more difficult.

Now the laboratory plans to determine which specific molecules and signaling pathways block recovery due to inflammation. The goal is to develop more precise therapeutic methods. For example, in the future, it might be possible to use monoclonal antibodies that would block a specific pathway hindering regeneration, thereby avoiding the need for broad immune suppression, which can be fraught with side effects.