Cell-specific spatial profiling of targeted protein expression to characterize the impact of intracortical microelectrode implantation on neuronal health.

Intracortical microelectrode arrays (MEAs) can record neuronal activity and advance brain-computer interface (BCI) devices. Implantation of the invasive MEA kills local neurons, which has been documented using immunohistochemistry (IHC). Neuronal nuclear protein (NeuN), a protein that lines the nuclei of exclusively neuronal cells, has been used as a marker for neuronal health and survival for decades in neuroscience and neural engineering.

Comprehensive proteomic analysis of the differential expression of 62 proteins following intracortical microelectrode implantation.

Intracortical microelectrodes (IMEs) are devices designed to be implanted into the cerebral cortex for various neuroscience and neuro-engineering applications. A critical feature of IMEs is their ability to detect neural activity from individual neurons. Currently, IMEs are limited by chronic failure, largely considered to be caused by the prolonged neuroinflammatory response to the implanted devices.

Depletion of complement factor 3 delays the neuroinflammatory response to intracortical microelectrodes.

The neuroinflammatory response to intracortical microelectrodes (IMEs) used with brain-machine interfacing (BMI) applications is regarded as the primary contributor to poor chronic performance. Recent developments in high-plex gene expression technologies have allowed for an evolution in the investigation of individual proteins or genes to be able to identify specific pathways of upregulated genes that may contribute to the neuroinflammatory response. Several key pathways that are upregulated following IME implantation are involved with the complement system.

Alternative splicing of CHEK2 and codeletion with NF2 promote chromosomal instability in meningioma.

Mutations of the NF2 gene on chromosome 22q are thought to initiate tumorigenesis in nearly 50% of meningiomas, and 22q deletion is the earliest and most frequent large-scale chromosomal abnormality observed in these tumors. In aggressive meningiomas, 22q deletions are generally accompanied by the presence of large-scale segmental abnormalities involving other chromosomes, but the reasons for this association are unknown. We find that large-scale chromosomal alterations accumulate during meningioma progression primarily in tumors harboring 22q deletions, suggesting 22q-associated chromosomal instability.