Brain, Nerve & Spinal Cord Injury
SPINAL CORD INJURY AND NERVE DAMAGE
Mechanism of Injury
Spinal cord and nerve damage can cause loss of motor and sensory function, resulting in significant patient disability. The exact physiologic mechanism underlying spinal cord injury is not fully understood but appears to involve several processes, including direct trauma, excitotoxicity, apoptosis, and inflammation. Crush injuries, usually from an automobile accident or fall, may result in direct physical trauma to neurons and supporting glial cells. Following a crush injury, excitatory amino acids such as glutamate are released and damage neurons by a mechanism called excitotoxicity. Apoptosis refers to programmed cell death following the injury. The final process to consider in treating spinal cord injury is damage caused by inflammatory cells. Directly after the injury, inflammatory cells migrate to the site of damage where they release factors that contribute to excitotoxicity, apoptosis, and oxygen based free radical damage, all which structurally limit the regrowth of nervous tissue. All of these processes lead to neuronal cell membrane damage which results in the loss of nerve cell function. Disruption of the conducting fibers interrupts the transmission of neural messages down the spinal cord, leading to drastic impairments and a reduced quality of life for spinal cord injury patients.
Maroon Biotech's Solution
Maroon’s surfactant chaperone technology can potentially have a huge impact on future spinal cord treatment. The cell membrane stabilizing and sealing capabilities of PEO-PPO-PEO copolymers allow it to mitigate several of the damaging reactions to spinal cord injuries. Because excitotoxicity results in membrane destabilization, a membrane stabilizer such as a PEO-PPO-PEO copolymer can sustain the viability of neural cells following this type of injury. It can also help limit damage caused by the inflammatory response because inflammatory changes and reperfusion injury destabilize membranes through peroxidation of membrane lipids and proteins. Finally, PEO-PPO-PEO copolymers can also help limit damage caused by the inflammatory response that may contribute to damaged membrane fluidity, helping severed neurons reconnect and thus allowing action potentials to travel once again through the damaged fiber. The actions of Maroon’s surfactant chaperone technology help retain and restore the functional capabilities of the nervous system and lead to improved post-injury motor skills and higher quality of life for spinal cord injury patients everywhere.
STROKE AND BRAIN TRAUMA
Mechanism of Injury
Many strokes occur when a clot blocks blood flow to a portion of the brain, preventing oxygen from reaching that area. Cells begin to die from lack of oxygen, creating a dying tissue mass called an infarct. Without treatment, this region grows and may result in life threatening complications due to its impact on brain function. The first priority in treatment is to restore blood flow to the brain. This is achieved by surgical intervention or administration of a thrombolytic drug. Reperfusion is, however, only the first step in the treatment of stroke. When blood flow is restored by reperfusion therapy, the sudden torrent of oxygen rich blood creates oxygen free radicals that increase the infarct damage. Despite use of clot busting drugs, there are still many serious post stroke complications that jeopardize patient’s lives and have serious implications for their quality of life. Some processes continue to damage the brain tissue with or without reperfusion treatment, and other processes damage the brain tissue as a direct result of reperfusion treatment. These damaging processes result in the formation of pores in neuronal cell membranes
Maroon Biotech's Solution
A therapy given along with mechanical or drug-based reperfusion techniques will help seal neuronal cell membranes and prevent further damage. Injected concurrently with reperfusion therapy, Maroon’s surfactant chaperone treatment will reduce damage to brain tissue. Injecting surfactant chaperones prevents much reperfusion injury from occurring and heals cells damaged by lack of oxygen, actually reducing the size of the original infarct. The combination therapy will have an even greater impact for stroke patients with reperfusion injury than for myocardial infarction (MI) patients with reperfusion injury because fewer treatment options exist for stroke patients. As with MI, the combination therapy will increase the likelihood of patient survival.
The beneficial effects of a PEO-PPO-PEO copolymer, Poloxamer-188, on nervous tissue have been shown in animal models. Neuroprotection has been demonstrated in the presence of a range of tissue trauma, including chemical agents and an excess of reactive oxygen species. Neuronal loss in brain slices is reduced, peroxidation of neurons by oxygen free radicals is inhibited, cell membranes are sealed, and loss of intracellular contents is arrested.