It’s thought that brain-computer interfaces could be used to treat a number of conditions, whether allowing a paralysed person to communicate with robotic limbs or to halt the symptoms of neurological disorders like epilepsy. However, they are usually rejected by the patient’s body before they begin to take effect.
A four-year study, which recently commenced at Case Western Reserve University on the back of a $1.8 million (£1.12 million) National Institutes of Health grant, aims to work out why this happens – and what can be done to prevent it.
According to lead researcher Jeffrey Capadona, brain implants provoke an inflammatory response that has “really limited the clinical application” of such devices to date.
“They work well in animal studies and show promise in clinical trials, but the devices don’t last long enough to really catch on. They fail at different rates for several reasons, but all fail.”
A preliminary study, undertaken in order to secure grant funding, outlined what tends to happen when an electrode is implanted in a patient’s brain. The procedure itself causes damage to nearby cells, provoking an immune system response coordinated by a gene called cluster of differentiation 14 (CD14). This causes inflammatory molecules to accumulate around the electrode and adjacent neurons to degenerate, creating a barrier between the implant and the healthy brain cells it needs to interact with.
The researchers believe the key to making brain-computer interfaces successful is to stop CD14 activity. They have already successfully demonstrated this model in mice. Similarly, it was found that overstimulating the gene causes neural recordings to suffer.
Professor Capadona now hopes that his team can identify a therapy suitable for inhibiting CD14 so that electrodes can be implanted without the adverse immune system response – similar to the anti-rejection drugs used by transplant patients.
“We have identified a drug that’s been approved for another clinical use, but which we believe patients can take and enable brain-computer interfaces to work longer,” he added.
source: epilepsyresearch
A four-year study, which recently commenced at Case Western Reserve University on the back of a $1.8 million (£1.12 million) National Institutes of Health grant, aims to work out why this happens – and what can be done to prevent it.
According to lead researcher Jeffrey Capadona, brain implants provoke an inflammatory response that has “really limited the clinical application” of such devices to date.
“They work well in animal studies and show promise in clinical trials, but the devices don’t last long enough to really catch on. They fail at different rates for several reasons, but all fail.”
A preliminary study, undertaken in order to secure grant funding, outlined what tends to happen when an electrode is implanted in a patient’s brain. The procedure itself causes damage to nearby cells, provoking an immune system response coordinated by a gene called cluster of differentiation 14 (CD14). This causes inflammatory molecules to accumulate around the electrode and adjacent neurons to degenerate, creating a barrier between the implant and the healthy brain cells it needs to interact with.
The researchers believe the key to making brain-computer interfaces successful is to stop CD14 activity. They have already successfully demonstrated this model in mice. Similarly, it was found that overstimulating the gene causes neural recordings to suffer.
Professor Capadona now hopes that his team can identify a therapy suitable for inhibiting CD14 so that electrodes can be implanted without the adverse immune system response – similar to the anti-rejection drugs used by transplant patients.
“We have identified a drug that’s been approved for another clinical use, but which we believe patients can take and enable brain-computer interfaces to work longer,” he added.
source: epilepsyresearch
