Professional Summary:
Hanadie Yousef is a trained neurobiologist and stem cell biologist with a focus on the mechanisms of aging, with pending and issued patents, several publications, a PhD from Berkeley, a 4-year postdoc at Stanford, experience leading research teams, and has worked in R&D at Regeneron and Genentech.

In graduate school, Yousef studied the role of adult stem cells in the biology of aging and developed methods for tissue rejuvenation in brain and muscle. Her current research in the Wyss-Coray lab lies in understanding the molecular and cellular mechanisms that contribute to both a decline in brain function with aging and the onset of neurodegenerative diseases, with a focus on understanding the interactions between aged blood and the blood-brain barrier.

Education and Research Training:
Hanadie Yousef earned her bachelors in Chemistry with honors and a minor in Spanish from Carnegie Mellon University (CMU) in 2008 and went on to obtain a Ph.D. in Molecular and Cell Biology at the University of California, Berkeley in 2013. Since April 2014 she has been a postdoctoral fellow in the Neurology department at Stanford University School of Medicine.

Undergraduate Research:
Yousef began doing biomedical research in high school, where she interned locally at a pharmaceutical company in New York, Regeneron, to do research on gene therapy and cancer. She presented her research in local and international science competitions and symposiums. She returned to Regeneron to continue her research during winter and summer internships for 5 years (2003-2008). During her undergraduate studies at CMU, Yousef did a research honors thesis at University of Pittsburgh Medical Center, where she elucidated molecular mechanisms driving idiopathic pulmonary lung fibrosis (2 co-authorship studies, 1 invention disclosure).

Dissertation Research:
Yousef studied the role of adult stem cells in the biology of aging and developed methods for tissue rejuvenation in brain and muscle (4, 1st author publications, 1 issued patent, 1 pending). During the last year of her graduate studies (2013), she did a summer internship at Genentech in the neurodegeneration group of R&D, where she studied inflammatory mechanisms underlying neurodegeneration.

Postdoctoral Research:
Yousef’s current research focus in the Wyss-Coray lab lies in understanding the molecular and cellular mechanisms that contribute to both a decline in brain function with aging and the onset of neurodegenerative diseases. She has a manuscript in review, a pending patent, and a translational research grant through the Stanford SPARK program based on her discoveries.

Ongoing collaborations with postdocs and scientists in the labs of: Professor Eugene Butcher (Immunology and Pathology), Professor Marion Buckwalter (Neurology and Neurosurgery), Professor Steven Quake (Bioengineering). Past collaboration with the Genetics Bioinformatics Service Center at Stanford. 

Hanadie has gotten many awards and honors along the way in pursuing her passion in translational scientific research, including the National Science Foundation graduate research fellowship (2009-2012), the NRSA F32 postdoctoral fellowship (2016-ongoing), a Stanford Spark grant (2017), presentation and poster awards, and travel and training scholarships at local and international scientific conferences and research institutions. Yousef has presented her research and given lectures across the globe, receiving attention in local, university and international media outlets. Yousef has a strong passion for teaching and mentorship. She was an Instructor for Drug Discovery at UCSC during the first 2 years of her postdoctoral training and has advised many undergraduate students during her graduate and postdoctoral research training, including 3 who received research honors theses under her tutelage. Yousef has several publications and issued and pending patents on methods for tissue rejuvenation.

Honors & Awards

  • NRSA F32 Postdoctoral Fellowship, NIH (division: National Institute on Aging) (2016-2019)
  • SPARK Scholar, Stanford spectrum award (2017)
  • National Science Foundation Graduate Research Fellowship, National Science Foundation (2009-2012)
  • Ellison Medical Foundation funded Molecular Biology of Aging course, Marine Biological Laboratories, Woods Hole, MA (July-August 2011)
  • Judith A. Resnik Award, Carnegie Mellon University (May 2008)
  • Keystone Symposia Scholarship Recipient, Keystone Symposia: Epigenetic and Metabolic Regulation of Aging and Aging-Related Diseases (May 2016)
  • Postdoc Poster Award for Translational Research, Bay Area Aging Meeting (BAAM), Gladstone Institutes, UCSF, San Francisco, CA (November 2016)
  • Poster Award: Alzheimer’s Researchers’ Symposium, Alzheimer’s Researchers’ Symposium: Gladstone Institutes, UCSF, San Francisco, CA (June 2015)
  • Graduate Poster Award for Translational Research, Bay Area Aging Meeting (BAAM), Gladstone Institutes, UCSF, San Francisco, CA (December 2014)
  • UCB Molecular and Cell Biology Department Travel Award, International Society for Stem Cell Research Conference in Boston, Ma (June 2013)
  • California Institute for Regenerative Medicine (CIRM) Travel Award, International Society for Stem Cell Research Conference in Toronto (June 2011)
  • HHMI Undergraduate Research Fellowships, Howard Hughes Medical Institute (2004-2005, 2007-2008)
  • Mitchell Scholarship in Chemistry, Carnegie Mellon University (2004)

Professional Education

  • Bachelor of Science, Carnegie Mellon University (2008)
  • Doctor of Philosophy, University of California Berkeley (2013)

Stanford Advisors


  • Hanadie Yousef, Irina M. Conboy, Michael J. Conboy, David V. Schaffer. "United States Patent 9,758,763 Methods and Compositions for Somatic Cell Proliferation and Viability", The Regents Of The University Of California, Sep 12, 2017


All Publications

  • Systemic attenuation of the TGF-ß pathway by a single drug simultaneously rejuvenates hippocampal neurogenesis and myogenesis in the same old mammal. Oncotarget Yousef, H., Conboy, M. J., Morgenthaler, A., Schlesinger, C., Bugaj, L., Paliwal, P., Greer, C., Conboy, I. M., Schaffer, D. 2015; 6 (14): 11959-11978


    Stem cell function declines with age largely due to the biochemical imbalances in their tissue niches, and this work demonstrates that aging imposes an elevation in transforming growth factor β (TGF-β) signaling in the neurogenic niche of the hippocampus, analogous to the previously demonstrated changes in the myogenic niche of skeletal muscle with age. Exploring the hypothesis that youthful calibration of key signaling pathways may enhance regeneration of multiple old tissues, we found that systemically attenuating TGF-β signaling with a single drug simultaneously enhanced neurogenesis and muscle regeneration in the same old mice, findings further substantiated via genetic perturbations. At the levels of cellular mechanism, our results establish that the age-specific increase in TGF-β1 in the stem cell niches of aged hippocampus involves microglia and that such an increase is pro-inflammatory both in brain and muscle, as assayed by the elevated expression of β2 microglobulin (B2M), a component of MHC class I molecules. These findings suggest that at high levels typical of aged tissues, TGF-β1 promotes inflammation instead of its canonical role in attenuating immune responses. In agreement with this conclusion, inhibition of TGF-β1 signaling normalized B2M to young levels in both studied tissues.

    View details for PubMedID 26003168

  • Age-Associated Increase in BMP Signaling Inhibits Hippocampal Neurogenesis STEM CELLS Yousef, H., Morgenthaler, A., Schlesinger, C., Bugaj, L., Conboy, I. M., Schaffer, D. V. 2015; 33 (5): 1577-1588


    Hippocampal neurogenesis, the product of resident neural stem cell proliferation and differentiation, persists into adulthood but decreases with organismal aging, which may contribute to the age-related decline in cognitive function. The mechanisms that underlie this decrease in neurogenesis are not well understood, although evidence in general indicates that extrinsic changes in an aged stem cell niche can contribute to functional decline in old stem cells. Bone morphogenetic protein (BMP) family members are intercellular signaling proteins that regulate stem and progenitor cell quiescence, proliferation, and differentiation in various tissues and are likewise critical regulators of neurogenesis in young adults. Here, we establish that BMP signaling increases significantly in old murine hippocampi and inhibits neural progenitor cell proliferation. Furthermore, direct in vivo attenuation of BMP signaling via genetic and transgenic perturbations in aged mice led to elevated neural stem cell proliferation, and subsequent neurogenesis, in old hippocampi. Such advances in our understanding of mechanisms underlying decreased hippocampal neurogenesis with age may offer targets for the treatment of age-related cognitive decline.

    View details for DOI 10.1002/stem.1943

    View details for Web of Science ID 000353292600019

    View details for PubMedID 25538007

  • Mechanisms of action of hESC-secreted proteins that enhance human and mouse myogenesis AGING-US Yousef, H., Conboy, M. J., Mamiya, H., Zeiderman, M., Schlesinger, C., Schaffer, D. V., Conboy, I. M. 2014; 6 (8): 602-620


    Adult stem cells grow poorly in vitro compared to embryonic stem cells, and in vivo stem cell maintenance and proliferation by tissue niches progressively deteriorates with age. We previously reported that factors produced by human embryonic stem cells (hESCs) support a robust regenerative capacity for adult and old mouse muscle stem/progenitor cells. Here we extend these findings to human muscle progenitors and investigate underlying molecular mechanisms. Our results demonstrate that hESC-conditioned medium enhanced the proliferation of mouse and human muscle progenitors. Furthermore, hESC-produced factors activated MAPK and Notch signaling in human myogenic progenitors, and Delta/Notch-1 activation was dependent on MAPK/pERK. The Wnt, TGF-β and BMP/pSmad1,5,8 pathways were unresponsive to hESC-produced factors, but BMP signaling was dependent on intact MAPK/pERK. c-Myc, p57, and p18 were key effectors of the enhanced myogenesis promoted by the hECS factors. To define some of the active ingredients of the hESC-secretome which may have therapeutic potential, a comparative proteomic antibody array analysis was performed and identified several putative proteins, including FGF2, 6 and 19 which as ligands for MAPK signaling, were investigated in more detail. These studies emphasize that a "youthful" signaling of multiple signaling pathways is responsible for the pro-regenerative activity of the hESC factors.

    View details for Web of Science ID 000345431000001

    View details for PubMedID 25109702

  • Let-7d microRNA affects mesenchymal phenotypic properties of lung fibroblasts AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY Huleihel, L., Ben-Yehudah, A., Milosevic, J., Yu, G., Pandit, K., Sakamoto, K., Yousef, H., LeJeune, M., Coon, T. A., Redinger, C. J., Chensny, L., Manor, E., Schatten, G., Kaminski, N. 2014; 306 (6): L534-L542


    MicroRNAs are small noncoding RNAs that inhibit protein expression. We have previously shown that the inhibition of the microRNA let-7d in epithelial cells caused changes consistent with epithelial-to-mesenchymal transition (EMT) both in vitro and in vivo. The aim of this study was to determine whether the introduction of let-7d into fibroblasts alters their mesenchymal properties. Transfection of primary fibroblasts with let-7d caused a decrease in expression of the mesenchymal markers α-smooth muscle actin, N-cadherin, fibroblast-specific protein-1, and fibronectin, as well as an increase in the epithelial markers tight junction protein-1 and keratin 19. Phenotypic changes were also present, including a delay in wound healing, reduced motility, and proliferation of fibroblasts following transfection. In addition, we examined the effects of transfection on fibroblast responsiveness to TGF-β, an important factor in many fibrotic processes such as lung fibrosis and found that let-7d transfection significantly attenuated high-mobility group-A2 protein induction by TGF-β. Our results indicate that administration of the epithelial microRNA let-7d can significantly alter the phenotype of primary fibroblasts.

    View details for DOI 10.1152/ajplung.00149.2013

    View details for Web of Science ID 000333328300007

    View details for PubMedID 24441869

  • hESC-secreted proteins can be enriched for multiple regenerative therapies by heparin-binding AGING-US Yousef, H., Conboy, M. J., Li, J., Zeiderman, M., Vazin, T., Schlesinger, C., Schaffer, D. V., Conboy, I. M. 2013; 5 (5): 357-372


    This work builds upon our findings that proteins secreted by hESCs exhibit pro-regenerative activity, and determines that hESC-conditioned medium robustly enhances the proliferation of both muscle and neural progenitor cells. Importantly, this work establishes that it is the proteins that bind heparin which are responsible for the pro-myogenic effects of hESC-conditioned medium, and indicates that this strategy is suitable for enriching the potentially therapeutic factors. Additionally, this work shows that hESC-secreted proteins act independently of the mitogen FGF-2, and suggests that FGF-2 is unlikely to be a pro-aging molecule in the physiological decline of old muscle repair. Moreover, hESC-secreted factors improve the viability of human cortical neurons in an Alzheimer's disease (AD) model, suggesting that these factors can enhance the maintenance and regeneration of multiple tissues in the aging body.

    View details for Web of Science ID 000320958800008

    View details for PubMedID 23793469

  • Inhibition and Role of let-7d in Idiopathic Pulmonary Fibrosis AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE Pandit, K. V., Corcoran, D., Yousef, H., Yarlagadda, M., Tzouvelekis, A., Gibson, K. F., Konishi, K., Yousem, S. A., Singh, M., Handley, D., Richards, T., Selman, M., Watkins, S. C., Pardo, A., Ben-Yehudah, A., Bouros, D., Eickelberg, O., Ray, P., Benos, P. V., Kaminski, N. 2010; 182 (2): 220-229


    Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and usually lethal fibrotic lung disease characterized by profound changes in epithelial cell phenotype and fibroblast proliferation.To determine changes in expression and role of microRNAs in IPF.RNA from 10 control and 10 IPF tissues was hybridized on Agilent microRNA microarrays and results were confirmed by quantitative real-time polymerase chain reaction and in situ hybridization. SMAD3 binding to the let-7d promoter was confirmed by chromatin immunoprecipitation, electrophoretic mobility shift assay, luciferase assays, and reduced expression of let-7d in response to transforming growth factor-beta. HMGA2, a let-7d target, was localized by immunohistochemistry. In mice, let-7d was inhibited by intratracheal administration of a let-7d antagomir and its effects were determined by immunohistochemistry, immunofluorescence, quantitative real-time polymerase chain reaction, and morphometry.Eighteen microRNAs including let-7d were significantly decreased in IPF. Transforming growth factor-beta down-regulated let-7d expression, and SMAD3 binding to the let-7d promoter was demonstrated. Inhibition of let-7d caused increases in mesenchymal markers N-cadherin-2, vimentin, and alpha-smooth muscle actin (ACTA2) as well as HMGA2 in multiple epithelial cell lines. let-7d was significantly reduced in IPF lungs and the number of epithelial cells expressing let-7d correlated with pulmonary functions. HMGA2 was increased in alveolar epithelial cells of IPF lungs. let-7d inhibition in vivo caused alveolar septal thickening and increases in collagen, ACTA2, and S100A4 expression in SFTPC (pulmonary-associated surfactant protein C) expressing alveolar epithelial cells.Our results indicate a role for microRNAs in IPF. The down-regulation of let-7d in IPF and the profibrotic effects of this down-regulation in vitro and in vivo suggest a key regulatory role for this microRNA in preventing lung fibrosis. Clinical trial registered with (NCT 00258544).

    View details for DOI 10.1164/rccm.200911-1698OC

    View details for Web of Science ID 000280206700013

    View details for PubMedID 20395557