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Al La Spada, MD PhD

Affiliations: 
1993-2009 University of Washington, Seattle, Seattle, WA 
 2009- Pediatrics University of California, San Diego, La Jolla, CA 
Area:
Polyglutamine disease mechanisms
Website:
https://profiles.ucsd.edu/albert.laspada
Google:
"Al La Spada"
Bio:

https://medschool.ucsd.edu/education/neurograd/faculty/Pages/albert-spada.aspx
Albert La Spada graduated Summa Cum Laude from the University of Pennsylvania with a degree in Biology in 1986. As a recipient of a Medical Scientist Training program award, he pursued combined M.D. - Ph.D. training at the University of Pennsylvania School of Medicine. His 'Molecular Biology' doctoral thesis research focused upon a neuromuscular disorder known as X-linked spinal & bulbar muscular atrophy (SBMA) or Kennedy's disease. While a graduate student, La Spada identified the cause of SBMA as an expansion of a trinucleotide repeat in the androgen receptor gene. As the first disorder shown to be caused by an expanded polyglutamine tract, this discovery of a novel type of genetic mutation has led to the emergence of new field of study in neurodegenerative disease. After completing his M.D. - Ph.D. training in 1993, Dr. La Spada became a Laboratory Medicine resident at the University of Washington Medical Center and then a Clinical Genetics fellow in the Division of Medical Genetics. He pursued postdoctoral fellowship training as a Howard Hughes Medical Institute Physician Fellow, continuing to focus upon neurodegenerative disease. He joined the faculty in the Department of Laboratory Medicine at the University of Washington Medical Center in 1998, and was a Professor of Laboratory Medicine, Medicine (Medical Genetics), Pathology, and Neurology (Neurogenetics). From 2004-2009, he was Director of the Center for Neurogenetics and Neurotherapeutics at the University of Washington. In 2009, Dr. La Spada accepted the position of Professor and Division Head of Genetics in the Departments of Pediatrics and Cellular & Molecular Medicine at the University of California, San Diego, and is a founding faculty member of the UCSD Institute for Genomic Medicine.
Dr. La Spada's research laboratory remains focused upon the molecular basis of neurodegenerative disease. Dr. La Spada's laboratory is attempting to understand the molecular events that underlie the processes of neurodegeneration and neuron cell death in spinocerebellar ataxia type 7 (SCA7), and has found a number of connections between pathways involved in transcription and neuron dysfunction. By reproducing molecular pathology in model organisms such as mice, he has also begun to use this mechanistic knowledge to develop therapies to treat this disorder. Dr. La Spada has been the recipient of numerous grants and awards from the National Institutes of Health, Howard Hughes Medical Institute, Muscular Dystrophy Association, Hereditary Disease Foundation, CHDI, Coulter Foundation, and American Federation for Aging Research. Among his funding awards is the prestigious Paul Beeson Physician Faculty Scholar Aging Research Award. In 2006, Dr. La Spada was inducted into the American Society for Clinical Investigation. In 2007, he was bestowed with the Lieberman Award by the Hereditary Disease Foundation for excellence in Huntington’s Disease research. Dr. La Spada sits on a variety of editorial boards and grant review committees
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Mean distance: 16.6 (cluster 11)
 
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Scott A. Wilke research assistant UCSD
Stephan J. Guyenet grad student 2009 University of Washington
Jamie Ann Johansen post-doc 2008-2010 UCSD
Stevan N. Djakovic post-doc 2010-2011 UCSD
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Publications

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Badders NM, Korff A, Miranda HC, et al. (2018) Selective modulation of the androgen receptor AF2 domain rescues degeneration in spinal bulbar muscular atrophy. Nature Medicine
Polanco MJ, Parodi S, Piol D, et al. (2016) Adenylyl cyclase activating polypeptide reduces phosphorylation and toxicity of the polyglutamine-expanded androgen receptor in spinobulbar muscular atrophy. Science Translational Medicine. 8: 370ra181
Guyenet SJ, Mookerjee SS, Lin A, et al. (2015) Proteolytic cleavage of ataxin-7 promotes SCA7 retinal degeneration and neurological dysfunction. Human Molecular Genetics. 24: 3908-17
Cortes CJ, La Spada AR. (2015) Autophagy in polyglutamine disease: Imposing order on disorder or contributing to the chaos? Molecular and Cellular Neurosciences. 66: 53-61
Ward JM, La Spada AR. (2015) Ataxin-3, DNA damage repair, and SCA3 cerebellar degeneration: on the path to parsimony? Plos Genetics. 11: e1004937
Eschbach J, von Einem B, Müller K, et al. (2015) Mutual exacerbation of peroxisome proliferator-activated receptor γ coactivator 1α deregulation and α-synuclein oligomerization. Annals of Neurology. 77: 15-32
Dubinsky AN, Dastidar SG, Hsu CL, et al. (2014) Let-7 coordinately suppresses components of the amino acid sensing pathway to repress mTORC1 and induce autophagy. Cell Metabolism. 20: 626-38
Ward JM, La Spada AR. (2014) Identification of the SCA21 disease gene: remaining challenges and promising opportunities. Brain : a Journal of Neurology. 137: 2626-8
Cortes CJ, Miranda HC, Frankowski H, et al. (2014) Polyglutamine-expanded androgen receptor interferes with TFEB to elicit autophagy defects in SBMA. Nature Neuroscience. 17: 1180-9
La Spada AR. (2014) Something wicked this way comes: huntingtin. Nature Neuroscience. 17: 1014-5
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