Our research strategy is unique. Most research projects are to find cures. We are looking for those in the medical research community to take Mark's research and discoveries and expand the available possible utilization possibilities for improved and more significant patient outcomes.
The Mark Egly Foundation desires to fund specific research with various uses of Alpha1 Antitrypsin to improve the health of individuals with and without other comorbidities. Comorbidities can be avoided with proper usage of Alpha1 Antitrypsin as a preventative measure to prevent disease development and the spread of disease.
The Mark Egly Foundation desires to fund specific research on the development of Alpha1 Antitrypsin through resources other than human blood and plasma donation.
We desire to fund research to have a more exact definition of what strictly medically defines and categorizes what Alpha1 Antitrypsin Deficiency is as a disease or condition.
We desire to fund studies with sound scientific rationale and clear relevance for people with Alpha1 Antitrypsin Deficiency but expand to the 152 Autoimmune diseases outlined in the Mark Egly patent filing of 2020 relating to a plurality of diseases and other previously unknown comorbidities. No idea is too novel for us to consider. We support academic and industry scientists, small biotech firms, big pharmaceutical companies, and medical care professionals. The spectrum of our desired research spans basic and clinical researchers.
Our Foundation has the desire to have our findings expanded to horizons with medical situations and diseases that were not previously considered relevant to Alpha1 Antitrypsin and its deficiency. Example - If there are insufficient levels of Alpha1 Antitrypsin to protect the tissue of the lungs, then there is logically not enough to protect Thrombospondin1 and other items that could affect the formation and development of proper blood cell formation in the bone marrow.
Mark desires for the Foundation to launch research into all the tissues that may be negatively affected by proteases like neutrophil elastase when they negligently attack any area of the body needlessly.
With Mark's discoveries that the protease inhibitor Alpha1 Antitrypsin is much more than just a defender of lung tissue associated with lung disease and Alpha1 Antitrypsin Deficiency.
With the Foundation, we can launch and investigate situations where prevention of many more conditions and deterioration of quality and valuable cells can be identified that need Alpha1 Antitrypsin protease inhibition to stop needless protease destruction of tissues and cells of any negative type.