Inflammation: A New Therapeutic Target Years After Stroke

Author: Institute for Neurological Research
Published: 2011/02/02 - Updated: 2022/06/19
Category Topic: Stroke - Academic Publications

Page Content: Synopsis - Introduction - Main

Synopsis: Breakthrough in stroke research identifying the potential reversibility of chronic neurologic disability in stroke survivors. The study utilized a new delivery method 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.

Defining Inflammation

Inflammation

Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective response involving immune cells, blood vessels, and molecular mediators. Inflammation can be either short-lived (acute) or long-lasting (chronic). In some diseases, like arthritis, your body's defense system and your immune system trigger inflammation when there are no invaders to fight off. In these autoimmune diseases, your immune system acts as if normal tissues are infected or somehow unusual, causing damage. Inflammation is a symptom of many chronic conditions, such as arthritis or Alzheimer's.

Introduction

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. All patients demonstrated improvement beginning within 10 minutes of drug administration(1).

Main Content

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).

Previous research had produced evidence of chronic brain inflammation following stroke.

The CNS Drugs results provide, for the first time, a 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. Currently, these patients lack treatment options to reverse the chronic disability that often results in many requiring 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 the enormous unmet medical need."

1. "Rapid Improvement in Chronic Stroke Deficits after Perispinal Etanercept: Three Consecutive Cases." CNS Drugs 2011; 25 (2): 145-155.

Attribution/Source(s): This quality-reviewed publication was selected for publishing by the editors of Disabled World (DW) due to its relevance to the disability community. Originally authored by Institute for Neurological Research and published on 2011/02/02, this content may have been edited for style, clarity, or brevity.