Neurology Central

GDF10 a potentially key player in stroke recovery

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New research carried out at the University of California Los Angeles (CA, USA) has verified the role of GDF10 in key repair mechanisms following stroke, consequently highlighting it’s potential therapeutic efficacy in aiding stroke recovery. The study was published recently in Nature Neuroscience.

Although previous studies have suggested the involvement of GDF10 in axonal sprouting following stroke, the mechanism underlying the process has remained unknown. Lead author S. Thomas Carmichael (University of California Los Angeles) and his team decided to investigate this further.

Utilizing animal models of stroke in addition to human autopsy tissue, the research team established that the activation of GDF10 occurred very soon following stroke. Further studies investigated the effect of GDF10 on axonal length in vitro in both stem-cell derived human neurons and rodent neurons, identifying that GDF10 did indeed play a significant role in stimulating axon growth.

Investigations into functional recovery, using stroke mouse models, also highlighted an association between increasing levels of GDF10 and recovery time following a stroke. Forced blocking of GDF10 reduced performance in motor tasks reinforcing the need for natural GDF10 levels for effective recovery.

“We were surprised by how consistently GDF10 caused new connections to form across all of the levels of analysis,” commented Carmichael.

Interestingly, despite it widely being believed that the mechanisms involved in brain development are similar to those of brain repair, findings indicated that GDF10 impacted entirely different genes following stroke than those involved with development.

“We found that regeneration is a unique program in the brain that occurs after injury. It is not simply Development 2.0, using the same mechanisms that take place when the nervous system is forming,” explained Carmichael.

Despite being in the early stages, the Neurological Institute of Neurological Disorders and Stroke (NINDS), who funded the study, are positive about the potential impacts of the research. Francesca Bosetti, stroke program director at NINDS commented: “These findings help to elucidate the mechanisms of repair following stroke. Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery.”

Source: NINDS press release

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