What is PRP?

Benefits of PRP

Scientists from the Gladstone Institute of Neurological Disease (GIND), UCSF, and Stanford have discovered that a certain type of collagen, collagen VI, protects brain cells against amyloid­beta (Aβ) proteins, which are widely thought to cause Alzheimer’s disease (AD). While the functions of collagens in cartilage and muscle are well established, it was unknown before this study that collagen VI is made by neurons in the brain and can fulfill important neuroprotective functions.

At baseline levels, platelets function as a natural reservoir for growth factors, including platelet­-derived growth factor (PDGF), epidermal growth factor (EGF), transforming growth factor­beta 1 (TGF­β1), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF), hepatocyte growth factor (HGF), and insulin-­like growth factor (IGF­I). There is a general consensus in PRP research that the injection of concentrated platelets, once activated, results in an exponential increase in numerous growth factors at the sight of PRP injection.

Intranasal PRP Procedure

PRP is harvested from the patient’s blood by a simple blood draw. During infusion, the patient will lay back on the exam table with their head tilted perpendicular to the ground. After local anesthetic is sprayed into the nose, the PRP combined with insulin and other nutrients is dripped up the nose with a special device. The patient will lie there for another 15 minutes while the PRP fuses into the brain. After this, the patient is free to get up and continue their daily activities.

To promote optimal regeneration, PRP is usually paired with several hyperbaric oxygen therapy (HBOT) sessions before and after. The PRP is infused the day before the intranasal stem cell infusion.

Why Insulin is Added to Intranasal PRP

Several mechanisms have been identified through which insulin administration may facilitate cognition, including regionally specific central nervous system (CNS) effects on glucose metabolism modulation of long­term potentiation (LTP), as well as modulation of CNS concentrations of neurotransmitters, such as norepinephrine and acetylcholine. However, peripherally administered insulin is not a viable treatment, in part due to risks associated with hypoglycemia.

Insulin and PRP can access the cerebrospinal fluid (CSF) along the olfactory neurons through the cribriform plate, or they can enter the CNS parenchyma through perivascular channels associated with the olfactory or trigeminal systems. In addition, a slower axonal transport pathway has been identified along which insulin can access the CNS several hours after intranasal administration.

A number of compounds, including insulin and insulin­-like growth factor­I, have been successfully delivered to the brain or CSF following intranasal administration. Intranasal insulin administration increases CSF insulin levels in humans about 10 minutes after the injection, with peak levels achieved in about 30 minutes. Blood glucose and insulin levels do not change after intranasal administration, demonstrating that the changes in CSF are not due to transport from the nasal cavity to the systemic circulation.

Intranasal insulin administration has facilitated verbal memory in adults with AD and mild cognitive impairment who were not APOE­ε4 carriers. For memory-­impaired ε4− adults, 10, 20, and 40 IU of insulin has improved declarative memory. The cognitive dose-­response curves for this group has shown that memory facilitation generally peaks at the 20 IU dose.*

*Results may vary: no guarantee of specific results

How Do Growth Factors in PRP Aid Healing?

PDGF (Platelet-Derived Growth Factor):

• Macrophage activation and angiogenesis
• Fibroblast chemotaxis and proliferative activity
• Enhances collagen synthesis
• Enhances the proliferation of bone cells

IGF­1 (Insulin-Like Growth Factor-­I):

• Chemotactic for myoblast and fibroblasts and stimulates protein synthesis
• Mediator in growth ad repair of skeletal muscle
• Enhances bone formation by proliferation and differentiation of osteoblasts

TGF­p (Transforming Growth Factor­β):

• Enhances the proliferative activity of fibroblasts
• Stimulates biosynthesis of type I collagen and fibronectin
• Induces deposition of bone matrix
• Inhibits osteoclast formation and bone resorption
• Regulation in balance between fibrosis and myocyte regeneration

PDEGF (Platelet-Derived Endothelial Growth Factor):

• Promotes wound healing by stimulating the proliferation of keratinocytes and dermal fibroblasts

PDAF (Platelet-Derived Angiogenic Factor)

• Induces vascularization by stimulating vascular endothelial cells

EGF (Endothelial Growth Factor):

• Cellular proliferation
• Differentiation of epithelial cells

VEGF (Vascular Endothelial Growth Factor)

• Angiogenesis
• Migration and mitosis of endothelial cells
• Creation of blood vessel lumen
• Creation of fenestrations
• Chemotactic for macrophages and granulocytes
• Vasodilation (indirectly by release of nitrous oxide)

HGF (Hepatocyte Growth Factor):

• Stimulates of hepatocyte proliferation and liver tissue regeneration
• Angiogenesis
• Mitogen for endothelial cells
• Antifibrotic

Scientific References

View our patent: US 2016/0235786 A1