Researchers from the University of Birmingham have shown that a medication candidate that penetrates the brain and is presently being developed as a treatment for cancer may also promote the regeneration of damaged neurons after spinal injury.
The findings of the study were just published today in the journal Clinical and Translational Medicine. Researchers demonstrated that the prospective medicine, which is known as AZD1390, may inhibit the response of nerve cells to DNA damage when it is given orally in animal models as well as in cell cultures. In addition, they hoped to demonstrate that it may stimulate the regeneration of injured nerves, therefore restoring both sensory and motor function after a lesion to the spinal cord.
This news comes only a few weeks after the same research team demonstrated that a different experimental medicine (AZD1236) may lessen the damage caused by spinal cord injuries by inhibiting the inflammatory response. Both of these researches were made possible through AstraZeneca’s Open Innovations Programme, which encourages the exchange of knowledge, compounds, tools, and technologies between the scientific community and AstraZeneca in order to speed up the process of drug discovery and development.
AstraZeneca is doing research on AZD1390 to investigate its potential to inhibit ATM-dependent signalling and the repair of DNA double strand breaks (DSBs). This action makes cancer cells more sensitive to the effects of radiation therapy. DNA damage, particularly double-strand breaks (DSBs) in the genome, which occur in numerous common malignancies and also after spinal cord injury, are what trigger the DNA Damage Response system, commonly known as the DDR.
The prolonged activation of this system was considered by specialists to hinder healing from a spinal cord injury. It was also anticipated that inhibiting this system would encourage nerve healing and help repair after an injury.
In their preliminary research, they discovered that AZD1390 promoted the proliferation of nerve cells in culture while at the same time inhibiting the ATM protein kinase pathway, which is an essential biochemical process that controls the body’s reaction to DNA damage.
After that, the researchers investigated the impact of AZD1390 after spinal cord damage by using animal models. In this study, the researchers demonstrated that administering AZD1390 orally resulted in a considerable reduction of the ATM protein kinase pathway, neuron regeneration beyond the site of damage, and the capacity of these nerves to transport electrical impulses over the location of the injury.
