Funded Research

Laboratory concept; Scientist uses a dropper to transfer chemical reagent to test tube. He observes the chemical reaction with a blurred background of research in the laboratory

NAAF’s research program funds investigations that advance the understanding of the mechanisms behind alopecia areata, help identify new therapeutic targets, provide information on the biological, psychosocial, and economic impacts, and further knowledge toward treatments and a cure. Since 1985, NAAF has awarded more than 208 research grants totaling more than $5.7 million. The studies we’ve invested in have enabled significant advances in research by helping to unravel the genetics of alopecia areata, identify important immune pathways, and yield clues to targeted treatments.

Find out about applying for a grant on the Research Grants and Awards page.

Role Of Autophagy In Alopecia Areata

Year: 2019 PI Name: Rupali Gund, PhD Award Type: Mentored Investigator Award Status: Completed Summary:
This project aims to understand the role of autophagy (a normal physiological process in the body that deals with destruction of cells in the body) in normal hair cycling and its role in the development of alopecia areata in the C3H/HeJ mouse model.

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Abstract:
Alopecia Areata (AA) is an organ-restricted autoimmune disease that specifically attacks the hair follicles, resulting in well-demarcated (AA Patchy) or diffuse non-scarring hair loss of the scalp (AA Totalis) or the entire body (AA Universalis). AA is a highly prevalent disease with a lifetime risk of 2.1%, however, the underlying disease mechanisms remain incompletely defined and under-studied. Histologically, AA presents as a “swarm of bees” in which inflammatory T lymphocytes attack the pigmented actively growing hair follicles. The prevalent notion for disease is thought to be the loss of immune privilege of hair follicles causing abnormal activation of pathogenic T cells. Genetic association studies previously conducted in our lab found several autophagy related genes associated with AA. In addition, our gene expression analysis revealed altered expression of autophagy related genes, prompting us to hypothesize that dysregulation of autophagy plays a critical role in AA pathogenesis. Autophagy is a survivalpromoting mechanism that involves capturing, degradation, and recycling of intracellular proteins and organelles in lysosomes. However, the contribution of autophagy in loss of hair follicle immune privilege and development of AA is not characterized. This project aims to understand the role of autophagy in normal hair cycling and its contribution to the development of alopecia in grafted C3H/HeJ mouse model.

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Impact: If successful, this study could provide new insights into the mechanism of alopecia areata pathogenesis mediated by autophagy and also identify novel targets for therapeutic intervention.