MYND: Unsupervised Evaluation of Novel BCI Control Strategies on Consumer Hardware

Neurophysiological studies are typically conducted in laboratories with limited ecological validity, scalability, and generalizability of findings. This is a significant challenge for the development of brain-computer interfaces (BCIs), which ultimately need to function in unsupervised settings on consumer-grade hardware. We introduce MYND: A framework that couples consumer-grade recording hardware with an easy-to-use application for the unsupervised evaluation of BCI control strategies. Subjects are guided through experiment selection, hardware fitting, recording, and data upload in order to self-administer multi-day studies that include neurophysiological recordings and questionnaires. As a use case, we evaluate two BCI control strategies ("Positive memories" and "Music imagery") in a realistic scenario by combining MYND with a four-channel electroencephalogram (EEG). Thirty subjects recorded 70.4 hours of EEG data with the system at home. The median headset fitting time was 25.9 seconds, and a median signal quality of 90.2% was retained during recordings.Neural activity in both control strategies could be decoded with an average offline accuracy of 68.5% and 64.0% across all days. The repeated unsupervised execution of the same strategy affected performance, which could be tackled by implementing feedback to let subjects switch between strategies or devise new strategies with the platform.Comment: 9 pages, 5 figures. Submitted to PNAS. Minor revisio

In Vivo Methods to Study Uptake of Nanoparticles into the Brain

Several in vivo techniques have been developed to study and measure the uptake of CNS compounds into the brain. With these techniques, various parameters can be determined after drug administration, including the blood-to-brain influx constant (Kin), the permeability-surface area (PS) product, and the brain uptake index (BUI). These techniques have been mostly used for drugs that are expected to enter the brain via transmembrane diffusion or by carrier-mediated transcytosis. Drugs that have limitations in entering the brain via such pathways have been encapsulated in nanoparticles (based on lipids or synthetic polymers) to enhance brain uptake. Nanoparticles are different from CNS compounds in size, composition and uptake mechanisms. This has led to different methods and approaches to study brain uptake in vivo. Here we discuss the techniques generally used to measure nanoparticle uptake in addition to the techniques used for CNS compounds. Techniques include visualization methods, behavioral tests, and quantitative methods

Liposomal Simvastatin Attenuates Neointimal Hyperplasia in Rats

Monocytes, macrophages, and inflammation play a key role in the process of neointimal proliferation and restenosis. The present study evaluated whether systemic and transient depletion of monocytes could be obtained by a single intravenous (IV) injection of simvastatin liposomes, for the inhibition of neointima formation. Balloon-injured carotid artery rats (n = 30) were randomly assigned to treatment groups of free simvastatin, simvastatin in liposomes (3 mg/kg), and saline (control). Stenosis and neointima to media ratio (N/M) were determined 14 days following single IV injection at the time of injury by morphometric analysis. Depletion of circulating monocytes was determined by flow cytometry analyzes of blood specimens. Inhibition of RAW264.7, J774, and THP-1 proliferation by simvastatin-loaded liposomes and free simvastatin was determined by the 3-(4, 5-dimethylthiazolyl-2)-2, 5- diphenyltetrazolium bromide assay. Simvastatin liposomes were successfully formulated and were found to be 1.5-2 times more potent than the free drug in suppressing the proliferation of monocytes/macrophages in cell cultures of RAW 264.7, J774, and THP-1. IV injection of liposomal simvastatin to carotid-injured rats (3 mg/kg, n = 4) resulted in a transient depletion of circulating monocytes, significantly more prolonged than that observed following treatment with free simvastatin. Administration to balloon-injured rats suppressed neointimal growth. N/M at 14 days was 1.56 ± 0.16 and 0.90 ± 0.12, control and simvastatin liposomes, respectively. One single systemic administration of liposomal simvastatin at the time of injury significantly suppresses neointimal formation in the rat model of restenosis, mediated via a partial and transient depletion of circulating monocytes