Grifols Announces Winners of the 10th Annual eALTA Research Fellowship at 2013 ERS Congress
- Awards fund early career investigators' research to advance understanding and treatment of alpha1-antitrypsin deficiency.
Barcelona, Spain – (September 9, 2013) – Grifols, a global healthcare company specializing in the production of biological therapies for rare genetic diseases, today announced the recipients of the 2013 European Alpha1 Antitrypsin Laurell's Training Awards (eALTA). The annual awards, sponsored exclusively by Grifols, provide two fellowships of €50,000 to young investigators whose research contributes to the understanding and treatment of alpha1-antitrypsin (AAT) deficiency. AAT deficiency is a rare, genetic condition in which low levels of the alpha1 protein can result in the early onset of emphysema and liver disease and can lead to disability and premature death.
The 2013 recipients of eALTA are Dr. Michael Emmet O'Brien of the Royal College of Surgeons in Ireland and Ms. Beata Poplawska of the National Institute of Tuberculosis and Lung Diseases in Poland. Dr. O'Brien and Ms. Poplawska were presented with the awards at the 2013 European Respiratory Society (ERS) Annual Congress in Barcelona during the Grifols-sponsored symposium.
Dr. O'Brien's research project will explore defective neutrophil degranulation in individuals with AAT deficiency. This transitional research aims to fully characterize the anti-degranulation effect of alpha1 antitrypsin AAT on the circulating neutrophils. Dr. O'Brien hopes to demonstrate that the neutrophils of AAT deficient individuals have disproportionate levels of activation, resulting in an increase of proteolytic enzymes that have been implicated as a major causative factor in pulmonary disorders that may present as severe exacerbations. The potential ramifications of AAT as a modulator of neutrophil degranulation provides a novel approach to the understanding of the role that AAT plays in healthy and AAT deficient individuals.
Ms. Poplawska's research will focus on the inhibitory activity of AAT genetic variants towards three related neutrophil serine proteinases: human neutrophil elastase (HNE), proteinase 3 (PR3) and cathepsin G (CG). HNE has been studied extensively in COPD and is generally well understood, but the role of PR3 and CG in lung tissue destruction is not clear and perhaps underestimated. Ms. Poplawska hopes to elucidate the effect that two common gene mutations, PiF and PiZ, have on inhibiting these neutrophil serine proteinases (NSP). Ms. Poplawska will also evaluate the concentration of both the NSPs and their inhibitors compared to the ‘normal' gene variant MM.
"Research initiatives such as eALTA help stimulate the interest and commitment of early-career scientists and clinicians to provide the basis for new therapies and treatment paradigms that ultimately benefit the alpha1 community" said Claus Vogelmeier, Professor of Internal and Respiratory Medicine at the Hospital of the Universities of Giessen and Marburg, Germany, and chair of the independent eALTA Review Team.
Grifols sponsors the eALTA awards to gain new insights into the epidemiology, pathophysiology and clinical treatment of AAT deficiency and associated disorders. Grifols is the global leader with augmentation therapies that are used to treat alpha1-antitrypsin deficiency and its commitment to research and continued support of early career scientists and clinicians is exemplified through the 10th anniversary of the eALTA research programs. To date, eALTA has awarded research grants totaling €875,000.
Although AAT deficiency is better understood today, there are still new discoveries being made, and the eALTA program is proud to support research in this important area.
The European Alpha1 Antitrypsin Laurell's Training Award supports basic and clinical research through two annual grants provided to early career investigators. The program is named in honor of Dr. Carl-Bertil Laurell, who first described alpha1-antitrypsin deficiency in 1963. The primary goal is to identify and support research projects that enhance the understanding of disease mechanisms of AAD deficiency, improve existing therapies, and identify potential new therapies. The eALTA program also encourages the entry of new clinicians and scientists into the field of AAT disorders and fosters collaborations among scientists in the field. For more information, go to http://www.ealta.eu/.
Grifols is a global healthcare company with a 70-year legacy of improving people's health and well-being through the development of life-saving plasma medicines, hospital pharmacy products, and diagnostic technology for clinical use.
As a leading producer of plasma medicines, Grifols has a presence in more than 100 countries and is the world leader in plasma collection, with 150 plasma donation centres across the US. Grifols is committed to increasing patient access to its life-saving plasma medicines through significant manufacturing expansions and the development of new therapeutic applications of plasma proteins. The company is headquartered in Barcelona, Spain, and employs more than 11,000 people worldwide.
In 2012, Grifols' sales exceeded 2,620 million euros. The company's class A shares are listed on the Spanish Stock Exchange, where they form part of the Ibex-35 (MCE:GRF). Its non-voting class B shares are listed on the Mercado Continuo (MCE:GRF.P) and on the US NASDAQ via ADRs (NASDAQ: GRFS). For more information visit www.grifols.com.
About Alpha1-Antitrypsin Deficiency
Alpha1-antitrypsin deficiency, also known as AAT deficiency or alpha1, is an inherited disorder that causes a significant reduction in the naturally occurring protein, alpha1-proteinase inhibitor. While rare, alpha1 is the most common cause of genetic emphysema in adults and the most common cause of liver disease in children. Individuals suffering from alpha1 often develop severe chronic obstructive pulmonary disease (COPD) leading to disability and premature death. Alpha1 is estimated to affect more than 100,000 people in Europe alone, although greater than 90% of individuals remain undiagnosed.
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