Keith Van Haren
Academic Appointments
- Instructor, Neurology & Neurological Sciences
Key Documents
Contact Information
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Clinical Offices
Division of Child Neurology 750 Welch Rd Ste 317 MC 5784 Palo Alto, CA 94304 Tel Work (650) 723-7299 Fax (650) 723-6841Practices at Lucile Packard Children's Hospital
- Academic Offices
Personal Information Tel (650) 723-6841
Professional Overview
Clinical Focus
- Leukodystrophies
- Autoimmune Diseases of the Nervous System
- Neurology - Child Neurology
Honors and Awards
- Scientific Award, Child Neurology Foundation (2011)
- Moore Award, Honorable Mention, American Association of Neuropathology (2003)
- Chief Resident, Stanford Dept Neurology (2009-2010)
- Medical Student Teaching Award, Stanford Dept Neurology (2009-2010)
- Commencement Speaker, University of Rochester School of Medicine (2005)
- Member, Arnold Gold Humanism Honor Society (2004)
Professional Education
| Board Certification: | Neurology - Child Neurology, American Board of Psychiatry and Neurology (2010) |
| Residency: | Stanford University - Dept of Neurology, CA USA (06/30/2010) |
| Internship: | Massachusetts General Hospital MA (06/30/2006) |
| Medical Education: | University of Rochester School of Medicine NY (2005) |
Scientific Focus
Current Research Interests
ALD is a monogenetic, X-linked disorder involving a gene (ABCD1) that encodes a peroxisomal protein. The biochemical hallmark of the disease is an accumulation of very-long chain fatty acids in several tissues, including myelin and blood. The disease has an estimated incidence of 1:20,000.
All ALD males manifest at least one of several overlapping phenotypes by early adulthood. The most severe phenotype, affecting about 2/3rds of patients, involves the abrupt onset of inflammatory demyelination that is typically fatal within a few years if left untreated. The origin of this phenotype is unknown; no phenotype-genotype correlation exists and risk factors remain undefined. Treatment for this form of the disease consists of hematopoietic stem cell transplantation that must be initiated in the early stages of demyelination to successfully halt disease progression.
We have recently identified serum vitamin D status as a risk factor for the onset of the inflammatory demyelinating phenotype of ALD. This has implications for pathogenesis and therapy. We are currently exploring the role of vitamin D at the macrophage-myelin interface. We are also developing data to support a clinical trial studying vitamin D as a preventive therapy in ALD boys without inflammatory demyelination.
Publications
- Case report of subdural hematoma in a patient with sturge-weber syndrome and literature review: questions and implications for therapy. J Child Neurol. 2013; (5): 672-5
- Identification of naturally occurring fatty acids of the myelin sheath that resolve neuroinflammation. Sci Transl Med. 2012; (137): 137ra73
- Immune response in leukodystrophies. Pediatr Neurol. 2007; (4): 235-44
- The unfolded protein response in vanishing white matter disease. J Neuropathol Exp Neurol. 2005; (9): 770-5
- The life and death of oligodendrocytes in vanishing white matter disease. J Neuropathol Exp Neurol. 2004; (6): 618-30
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