Cells: Hemostemix ACP-01 and NCP-01 Provides the Scientific Basis for Improving the Longevity and Signal Uptake of Brain Computer Implants

Implantable electrodes within the brain have enabled remarkable achievements—e.g., paralyzed individuals playing chess and blind individuals recognizing letters. However, these devices often fail between six months and one year. The longest BCI in use lasted seven years. Even then, issues like inflammation, scarring, and programmed cell death (apoptosis) undermine performance over time.

The article proposes using two types of autologous (patient-derived) progenitor cells: Angiogenic Cell Precursors (ACP-01, VesCell™) and Neural Cell Precursors (NCP-01), delivered into the cerebrospinal fluid, to foster a healing cellular environment around the implant.

• ACP-01 (VesCell™) produces signals like IL-8, VEGF, and angiogenin. They attract natural killer (NK) cells that suppress inflammation, reduce tissue scarring, and support new blood vessel growth (angiogenesis).
• ACP-01potentiate healing through the expression of tissue regeneration factors CXCL8, VEGF, and angiogenin. They include CD34+ (blood stem cell). CXCL8 recruit endogenous CD34+, that circulate peripherally, to the site of implant.
• CXCL8 (interleukin-8) activate NF-κB, resulting in gene transcription and protein synthesis necessary for learning (memory formation and consolidation).
• NCP- 01express receptors like CXCR4 and migrate toward the BCI site. NCP help shift immune cells into a neuroprotective (M2) state. NCP differentiate into neurons and supporting glial cells that promote new synaptic connections and neural plasticity.

Together, ACP and NCP support a cascade of beneficial molecular events:

• Activation of neurotrophic factors and NF-κB pathways that protect cells (anti-apoptosis).
• Promotion of synaptogenesis (formation of connections between neurons), neuritogenesis (growth of neural processes), to improve learning-related plasticity.
• As the patient’s DNA-based engineered cellular environment, ACP and NCP home to the site of BCI, decrease inflammation, increase angiogenesis, increase neuro-protectiveness, promote new synaptic connections, and may dramatically extend the lifespan of BCI, signal fidelity and learning.

Hemostemix’s patented proprietary platform produces ACP-01 (angiogenic precursors) and NCP-01 (neural precursors) from a patient’s own blood. This new research provides a scientific basis of how the combination of ACP-01+NCP-01 promises to overcome the major limitations in BCI implants.

• The findings align with Hemostemix’s vision of licensing ACP-01 and NCP-01 to enhance BCI longevity and functionalities.

This research paves the way for:

• Licensing with BCI technology companies to combine autologous stem-cell support of BCI with cutting-edge patient-based angiogenic and neural interfaces.
• Rapid preclinical and clinical testing of ACP-01 + NCP-01 at BCI implant sites.

“We envision each patient’s own stem cell as the ultimate substrate for the brain/AI interface, constitutively augmenting the cellular milieu to improve the longevity of signal fidelity and ultimately facilitate machine learning and memory” stated Dr. Fraser Henderson, lead author.

“I want to thank Dr. Henderson and Ms. Tuchman for this very thorough exposition of the benefits of using one’s own DNA structured as ACP & NCP to improve BCIs. Truly, this is incredible work. Coupled with our market analyses of the top three BCI companies, shareholders can expect more news to follow, as Mr. Lawrence, Chief Commercialization Officer and I meet with potential partners,” stated Thomas Smeenk, CEO.

Dr. Henderson has outlined a new cell-based approach that may allow brain implants to work reliably for years. By delivering two types of the patient’s blood-derived stem cell precursors—one that fights inflammation and boosts blood flow, the other that helps build new neuronal cells—this method could protect and improve the brain at the site of BCI implant. Hemostemix’s ready-to-use cell products (ACP-01 and NCP-01) are a direct fit for this approach and could potentially transform how long and well brain-computer interfaces function.