LOS ANGELES, CA – February 1 2011 – A breakthrough in stroke research identifying the potential reversibility of chronic neurologic disability in stroke survivors has published today. In the February 1, 2011 issue of the journal CNS Drugs the first human results of a new method of targeting chronic brain inflammation years after stroke are reported. Rapid improvement in impaired motor function, gait, hand function, sensory deficits, spatial perception, speech, cognition and behavior were noted among the first three consecutive patients treated. All patients demonstrated improvement beginning within 10 minutes of drug administration(1).
The study utilized a new method of delivery of etanercept, a potent biotechnology anti-inflammatory therapeutic. Etanercept has been a breakthrough for rheumatoid arthritis and other inflammatory disorders. It works by neutralizing tumor necrosis factor (TNF), a cytokine that initiates and amplifies inflammation. The therapeutic potential of etanercept in Alzheimer’s disease, traumatic brain injury, spinal cord injury, sciatica, and other neuroinflammatory disorders has attracted increasing attention(1-4).
Previous research had produced evidence of chronic brain inflammation following stroke. The CNS Drugs results provide, for the first time, proof-of-concept that targeting chronic brain inflammation is a viable therapeutic approach in humans years after stroke. The medical need is massive; in the United States alone approximately 795,000 individuals suffer a new or recurrent stroke each year. This calculates to a stroke happening every 40 seconds. At present, these patients lack treatment options to reverse the chronic disability that often results and many require full time care.
These new results provide a new direction for stroke research. In their most recent consensus statement, “Stroke: Working Towards a Prioritized World Agenda”, leading stroke researchers recognized the need to “scan the scientific landscape to embrace new ideas and approaches …[and] think outside the box … could advances in the understanding of … inflammation dramatically change our thinking about stroke pathogenesis?”
“The possibility of a leap in our understanding of brain dysfunction caused by stroke by exploring inflammatory pathways was anticipated by the forward-thinking stroke research community,” said Edward Tobinick MD, the author of the study and inventor of the etanercept delivery method. “There is potential to address enormous unmet medical need.”
1. “Rapid Improvement in Chronic Stroke Deficits after Perispinal Etanercept: Three Consecutive Cases”. CNS Drugs 2011; 25 (2): 145-155. A video documenting the rapid effect of treatment accompanies the article at http://www.vimeo.com/18550399.
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Scientific notes
1. Tobinick, E. Rapid Improvement in Chronic Stroke Deficits after Perispinal Etanercept: Three Consecutive Cases. CNS Drugs 2011; 25 (2): 145-155
2. Increasing scientific evidence suggests the therapeutic potential of etanercept and related anti-TNF therapeutics for treatment of neuroinflammatory disorders.
- Perispinal etanercept: a new therapeutic paradigm in neurology. Expert Rev Neurother 2010; 10 (6): 985-1002
- Therapeutic evaluation of etanercept in a model of traumatic brain injury. J Neurochem 2010; 115 (4): 921-929
- Tumor Necrosis Factor-Alpha Antagonist Reduces Apoptosis of Neurons and Oligodendroglia in Rat Spinal Cord Injury. Spine (2011); (in press)
- Attenuation of Inflammatory Events in Human Intervertebral Disc Cells with a Tumor Necrosis Factor Antagonist. Spine (2011); in press (2011)
- Randomized, double-blind, placebo-controlled, dose-response, and preclinical safety study of transforaminal epidural etanercept for the treatment of sciatica. Anesthesiology 2009; 110 (5): 1116-1126
- Immediate Anti-Tumor Necrosis Factor-Alpha (Etanercept) Therapy Enhances Axonal Regeneration After Sciatic Nerve Crush. J Neurosci Res 2010; 88 (2): 360-368
- Anti-TNF Therapy in the Injured Spinal Cord. Trends Pharmacol Sci 2011; (in press). 3. Elevated levels of TNF in the brain and blood of ischemic stroke patients were earlier identified as correlating with stroke size.
- Zaremba J, Skrobanski P, Losy J. Tumour Necrosis Factor-Alpha is Increased in the Cerebrospinal Fluid and Serum of Ischaemic Stroke Patients and Correlates with the Volume of Evolving Brain Infarct. Biomed Pharmacother 2001; 55 (5): 258-263
4. Inflammatory mechanisms, including TNF elevation, had earlier been identified as a potential therapeutic target in animal stroke models, particularly in the stroke penumbra.
- Kaushal V, Schlichter LC. Mechanisms of Microglia-Mediated Neurotoxicity in a New Model of the Stroke Penumbra. J Neurosci 2008; 28 (9): 2221-2230
- Price CJ, Wang D, Menon DK et al. Intrinsic Activated Microglia Map to the Peri-Infarct Zone in the Subacute Phase of Ischemic Stroke. Stroke 2006; 37 (7): 1749-1753
- Inflammation as a therapeutic target in acute ischemic stroke treatment. Curr Top Med Chem 2009; 9 (14): 1240-1260
