Dr. Albert La Spada, MD, Ph.D, FACMGG
Bio
Albert La Spada graduated Summa Cum Laude from the University of Pennsylvania with a degree in Biology in 1986. While a M.D. - Ph.D. student at the University of Pennsylvania School of Medicine, La Spada identified the cause of X-linked spinal & bulbar muscular atrophy (SBMA) as an expansion of a trinucleotide repeat in the androgen receptor gene. As the first disorder shown to be caused by an expanded repeat tract, this discovery of a novel type of genetic mutation led to the emergence of a new field of study. After completing training as a Clinical Genetics fellow and a Howard Hughes Medical Institute Physician Postdoctoral Fellow, he joined the faculty at the University of Washington Medical Center in 1998, and became a Professor of Laboratory Medicine, Medicine (Medical Genetics), and Neurology (Neurogenetics). In 2009, Dr. La Spada accepted the position of Professor and Division Head of Genetics in Pediatrics, Cellular & Molecular Medicine, and Neurosciences at the University of California, San Diego, and was a founding faculty member of the UCSD Institute for Genomic Medicine and Sanford Consortium for Regenerative Medicine. Dr. La Spada was recruited as the founding Director of the Duke Center for Neurodegeneration & Neurotherapeutics, was appointed Distinguished Professor of Neurology, Neurobiology, and Cell Biology, and held the Lincoln Financial Endowed Chair at the Duke University School of Medicine.
In 2020, Dr. La Spada joined the faculty of the University of California Irvine as Distinguished Professor of Pathology & Laboratory Medicine and Neurology, and he founded the UCI Center for Neurotherapeutics which he directs. In 2023, Dr. La Spada was appointed as the Jack W. Peltason Endowed Chair by the Chancellor of the University of California Irvine in recognition of his academic accomplishments and commitment to collaborative research. Dr. La Spada's research is focused upon neurodegenerative disease, and he is seeking the molecular genetic events that underlie neuron dysfunction in SBMA, Huntington’s Disease, spinocerebellar ataxia type 7 (SCA7), SCA2, ALS, Parkinson’s disease, and Alzheimer’s disease. He and his team have uncovered evidence for transcription dysregulation, perturbed bioenergetics, and altered protein quality control as contributing factors to cellular dysfunction in CNS diseases. By reproducing molecular pathology in mice and in neurons and other cell types derived from human patient stem cells, Dr. La Spada has begun to develop therapies to treat these disorders.
