Huda Yahya Zoghbi (Arabic: هدى الهبري الزغبي Hudā al-Hibrī az-Zughbī; born Huda El-Hibri; 20 June 1954) is a Lebanese-born American geneticist, and a professor at the Departments of Molecular and Human Genetics, Neuroscience and Neurology at the Baylor College of Medicine. She is the director of the Jan and Dan Duncan Neurological Research Institute. She was the editor of the Annual Review of Neuroscience from 2018 to 2024. Her work helped elucidate the genes and genetic mechanisms responsible for a number of devastating neurological disorders, such as Rett syndrome and spinocerebellar ataxia type 1. Zoghbi's discoveries have provided new ways of thinking about other neurological disorders such as Parkinson's disease, Alzheimer's, autism and intellectual disability, which could lead to new therapeutics and better, more efficient treatments. In 2017, she was awarded the Canada Gairdner International Award and the Breakthrough Prize in Life Sciences. She shared the 2020 Brain Prize with Adrian Bird for their work on Rett syndrome, and shared the 2022 Kavli Prize in Neuroscience, awarded "for pioneering the discovery of genes underlying a range of serious brain disorders".
Early life and education Huda Zoghbi was born in Beirut, Lebanon on 20 June 1954, and raised in Beirut. She loved reading works by William Shakespeare, Jane Austen and William Wordsworth in high school and intended to pursue literature at university. Her mother convinced her to study biology instead, on the grounds that 'a woman growing up in the Middle East should pick a career ensuring independence and security, while she can always write on the side'. Zoghbi was admitted as a biological sciences major at the American University of Beirut (AUB) in 1973 and entered the university's medical school 2 years later. The Lebanese Civil War began in 1976 during her first year of medical school. Although she and her classmates decided to stay at the university, after her brother was injured by shrapnel, their parents sent them to live with their sister in Austin, Texas, with plans to return the following summer. The war, however, raged on, and Zoghbi was under the impression that school terms at American medical schools began in October, as was the case with Lebanese schools. However, in October, it was confirmed that she was still unable to return to Lebanon due to the war, and US medical schools had begun their fall term 2 months earlier. Her family friends in America suggested she apply to Vanderbilt University. Vanderbilt did not accept transfer students, but recommended Meharry Medical College instead; Meharry accepted her on the spot. Despite her continued desire to return to Lebanon the next summer, on the advice of professors at AUB, she stayed at Meharry and earned an MD degree in 1979, after which she joined the Texas Children's Hospital at the Baylor College of Medicine as a pediatric resident. Zoghbi initially intended to specialise in pediatric cardiology. During her rotation at pediatric neurology, Marvin Fishman, the head of the division, convinced her that the brain was more interesting than the heart. She then started a 3-year term as a postdoctoral researcher in pediatric neurology after she finished her residency in 1982.
Career
From 1982 to 1985, Zoghbi was a postdoctoral researcher in pediatric neurology at the Baylor College of Medicine. She became an assistant professor at the Department of Pediatrics at Baylor in 1988, and was successively promoted to associate professor in 1991 and professor in 1994. At present, Zoghbi is a professor at the Department of Molecular and Human Genetics at Baylor, with appointments as a professor at the Department of Neuroscience and the Department of Pediatrics Section of Neurology and Developmental Neuroscience, the Ralph Feigin, M.D. Endowed Chair, the director of the Texas Children's Hospital Jan and Dan Duncan Neurological Research Institute, a member of the Dan L. Duncan Comprehensive Cancer Center at Baylor, and an investigator at the Howard Hughes Medical Institute. She is also a member of the board of directors of Regeneron Pharmaceuticals. She also served on the Life Sciences jury for the Infosys Prize in 2014.
Research In 1983, Zoghbi learnt of Rett syndrome from Bengt Hagberg's account in Annals of Neurology. The paper allowed Zoghbi to diagnose a five-year-old she treated at Texas Children's Hospital, and a week later she saw another patient with the same set of symptoms. When she investigated medical records, she found more cases of Rett syndrome that had been misdiagnosed. This sparked her interest in Rett syndrome, at a time when there was no report of the disease in the US. An article she published in 1985 attracted many Rett syndrome patients to Texas Children's Hospital, giving her access to a large number of cases. Since most patients of Rett syndrome were girls, and symptoms were very consistent across patients, Zoghbi believed genetics were involved in the disease process. This led her to join Arthur Beaudet's group in 1985, after finishing her term as a postdoctoral researcher, for training in genetics and molecular biology. Beaudet advised against Rett syndrome as her research project since its mode of inheritance was still not obvious, and recommended a more approachable problem – spinocerebellar ataxia type 1, a dominantly inherited neurological disorder. In 1988, Zoghbi left Beaudet's group and founded her own lab at Baylor. In addition to her research on spinocerebellar ataxia type 1 and Rett syndrome, Zoghbi is participating in a joint research collaboration into CDKL5 Deficiency Disorder, funded by the Loulou Foundation, Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute (NRI) at Texas Children's Hospital
Spinocerebellar ataxia type 1 Following the establishment of her own lab, Zoghbi continued studying spinocerebellar ataxia type 1 (SCA1), in collaboration with Harry Orr from the University of Minnesota. On the same day, 8 April 1993, both Zoghbi and Orr identified ATXN1 as the gene responsible for SCA1. They determined that the disease was caused by an expansion of the glutamine-encoding CAG trinucleotide repeat in this gene, and that the younger the age of onset, the longer the CAG repeat. Further work by Zoghbi, Orr and their teams demonstrated that the misfolding, aggregation, and proteasomal degradation of the protein product of this gene, Ataxin 1, played a role in the disorder.
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