Silicon electronics could revolutionize brain implants

Implanted electrode devices that stimulate the brain are used to mitigate the effects of Parkinson's, epilepsy and other neurodegenerative conditions. Current devices only use a few electrodes, and the number of patients with such implants is limited by the invasiveness of the implantation process and the large size of the device. A less invasive implant with more channels could enable radical improvements in brain-machine interfaces. Ken Shepard from Columbia Engineering is leading a multi-site research team to develop such a device, funded by a four-year $15.8m grant from DARPA. The researchers aim to create an implantable brain-interface device with one million channels to enable recording from and stimulation of the sensory cortex. At the end of the four-year programme, they plan to apply for regulatory approval to begin experiments in humans.

"This is a very aggressive timeline," Shepard noted. "We think the only way to achieve this is to use an all-electrical approach that involves a massive surface-recording array with more than one million electrodes fabricated as a monolithic device on a single CMOS integrated circuit." The implanted chips will be light, flexible enough to move with the tissue, and use wireless powering and data telemetry. "By using the state-of-the-art in silicon nanoelectronics and applying it in unusual ways, we are hoping to have a big impact on brain-computer interfaces. If we are successful, the tiny size and massive scale of this device could provide the opportunity for transformational interfaces to the brain, including direct interfaces to the visual cortex that would allow patients who have lost their sight to discriminate complex patterns at unprecedented resolutions," said Shepard.

Brain stimulation speeds walking in Parkinson's patients

Non-invasive brain stimulation and physical therapy – alone or in combination – improve some measures of walking ability in patients with Parkinson's disease. That’s the conclusion of a clinical trial headed up by Krisna Piravej and colleagues at Chulalongkorn University in Thailand. The study included 60 patients with slow walking speed due to Parkinson's disease. Patients were randomly assigned to three groups. One group received transcranial direct current stimulation (tDCS), which delivers a mild electrical current through the brain, with the goal of stimulating neural networks involved in motor coordination. Patients received six 30-minute tDCS sessions over two weeks. The second group received a physical therapy program, while the third received both tDCS and physical therapy (Am. J. Phys. Med. Rehabil. doi: 10.1097/PHM.0000000000000783).

The researchers used a computerized motion capture system to perform gait analysis before and after treatment. The three groups exhibited similar and significant improvement in some measures of gait. Walking speed increased by an average of about 19%, with only minor differences between groups. Step length increased by approximately 12%. Both improvements lasted for at least eight weeks after the end of treatment. While deep brain stimulation is an effective treatment for slow walking and other manifestations of Parkinson's, its use is limited by the risk of complications from surgery to place the brain electrodes. As a non-invasive, non-surgical procedure, with electrical stimulation delivered via electrodes placed on the scalp, tDCS avoids these risks. In the study, a few patients experienced a burning sensation during tDCS; no other complications were observed.

Scientists probe function of cerebellar interneurons

Researchers at the Max Planck Florida Institute for Neuroscience (MPFI) are investigating how different types of cells in the cerebellum have distinct roles in motor behaviour. The cerebellum, an area of brain involved in movement, comprises several distinct types of neurons. Purkinje cells are the only neurons that send information outside of the cerebellum, thus any cerebellar involvement in motor activity must be driven by the firing rates of these cells. The output of Purkinje cells, however, is influenced by neighbouring cells, including local inhibitory interneurons located in the molecular layer. Understanding how these interneurons contribute to cerebellar function and motor behaviour could help identify new ways to treat debilitating movement conditions, but they are difficult to study in isolation. The solution developed by the MPFI team involved use of a gene that’s uniquely expressed by interneurons of the molecular layer, but not expressed in neighbouring cells (PLoS ONE 12 e0179347).

To selectively target and control interneurons of the cerebellar molecular layer, the researchers used a genetically engineered mouse model, which exploits a unique gene encoding c-Kit to differentiate interneurons from other cell types. C-Kit is a protein robustly expressed by inhibitory interneurons of the cerebellar molecular layer, but weakly expressed by other cerebellar cell types, such as mature Purkinje cells. By using the c-kit mice, the team could specifically access molecular layer interneurons and manipulate their activity in vitro, using both optogenetic and chemogenetic methods. The technique should be able to provide similarly exciting results in vivo studies in the future. "Our new method has transformed the research that we're doing," said research fellow Matt Rowan, who is already working on further projects employing these mice.

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