Ola A. Awad, PhD

• Suez Canal University, School of Medicine, Egypt, MBBCh, Medicine and Surgery, 1992
• Suez Canal University, School of Medicine, Egypt, M.Sc, Histology and Cell Biology, 2001
• University of Iowa, School of Medicine, IA, PhD, Anatomy and Cell Biology, 2007
• Johns Hopkins School of Medicine, MD, Postdoctoral training, Pediatric Oncology, 2009
• University of Maryland School of Medicine, MD, Postdoctoral training, Neurodegeneration, 2014

Dr. Awad’s research area is the use of human stem cells in regenerative medicine and disease modeling. Her previous work aimed at optimizing the use of hematopoietic stem cells for treatment of diabetic vascular complications, which uncovered a new mechanism of diabetes-induced stem cell dysfunction through modulation of inflammatory response. During her postdoctoral studies, Dr Awad’s research led to the identification of a cancer stem cell population in Ewing’s sarcomas (EWS), the second most common bone tumors in children and young adults. She also tested the use of novel therapeutic molecules against EWS/FLI1 oncogene to overcome EWS stem cell chemo-resistance and prevent tumor relapse.

Currently, Dr. Awad’s research focuses on the use of human induced-pluripotent stem cells (iPSCs) to investigate mechanisms responsible for neurodegeneration in Parkinson's Disease (PD). Her research uncovered a novel mechanism by which GBA1 mutations, the most common genetic risk factor for PD result in lysosomal dysfunction, through deregulation of the transcription factor EB (TFEB), the master regulator of lysosomal biogenesis and autophagy. Her laboratory is currently studying the effects of GBA1-mediated deregulation of mTORC1-TFEB axis on mitochondrial homeostasis and endoplasmic reticulum stress in PD. Her long-term goal is to develop novel therapies capable of preventing neuronal loss, which can have a significant impact not only on PD but also on many other neurodegenerative disorders.

Neurodegeneration, GBA1 mutations, Parkinson's disease, Induced-pluripotent stem cells, autophagy, lysosomal biogenesis, transcription factor EB (TFEB), mTOR kinase.

• Awad O, Sarkar C, Panicker LM, Miller D, Zeng X, Sgambato JA, Lipinski MM, Feldman RA. (2015) Altered TFEB-mediated lysosomal biogenesis in Gaucher disease iPSC-derived neuronal cells. Hum Mol Genet.15;24(20):5775-88.
• Brown RA, Voit A, Srikanth MP, Thayer JA, Kingsbury TJ, Jacobson MA, Lipinski MM,
  Feldman RA, Awad O. (2019) mTOR hyperactivity mediates lysosomal dysfunction in
  Gaucher’s disease iPSC- neuronal cells. Dis Model Mech. 2019 Oct 16;12(10).
• Thayer, J.A., Awad, O., Hegdekar, N., Sarkar, C., Tesfay, H., Burt, C., Zeng, X., Feldman,
  R.A. and Lipinski, M.M. (2020) The PARK10 gene USP24 is a negative regulator of autophagy and ULK1 protein stability. Autophagy, 16(1):140-152. PMID: 30957634.