# Angiogenic Cell Precursors and Neural Cell Precursors in Service to the Brain–Computer Interface

## TL;DR

This paper proposes using angiogenic and nerve cell precursors to improve brain-computer interfaces by reducing inflammation and supporting neural function.

## Contribution

The novelty lies in proposing a biomolecular strategy using ACPs and NCPs to enhance BCI performance and longevity.

## Key findings

- Implanted BCI electrodes cause inflammation, scarring, and signal degradation over time.
- ACPs and NCPs may suppress inflammation and promote neural repair and plasticity.
- The proposed strategy could extend BCI functionality beyond current limitations.

## Abstract

The application of artificial intelligence through the brain–computer interface (BCI) is proving to be one of the great advances in neuroscience today. The development of surface electrodes over the cortex and very fine electrodes that can be stereotactically implanted in the brain have moved the science forward to the extent that paralyzed people can play chess and blind people can read letters. However, the introduction of foreign bodies into deeper parts of the central nervous system results in foreign body reaction, scarring, apoptosis, and decreased signaling. Implanted electrodes activate microglia, causing the release of inflammatory factors, the recruitment of systemic inflammatory cells to the site of injury, and ultimately glial scarring and the encapsulation of the electrode. Recordings historically fail between 6 months and 1 year; the longest BCI in use has been 7 years. This article proposes a biomolecular strategy provided by angiogenic cell precursors (ACPs) and nerve cell precursors (NCPs), administered intrathecally. This combination of cells is anticipated to sustain and promote learning across the BCI. Together, through the downstream activation of neurotrophic factors, they may exert a salutary immunomodulatory suppression of inflammation, anti-apoptosis, homeostasis, angiogenesis, differentiation, synaptogenesis, neuritogenesis, and learning-associated plasticity.