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Keith Van Haren, MD

Academic Appointments

  • Assistant Professor of Neurology at the Stanford University Medical Center

Key Documents

Contact Information

  • Clinical Offices
    Child Neurology 730 Welch Rd Ste 206 Palo Alto, CA 94304
    Tel Work (650) 723-0993 Fax (650) 721-6350
  • Academic Offices
    Personal Information
    Tel (650) 723-0993


Clinical Focus

  • Leukodystrophies
  • Autoimmune Diseases of the Nervous System
  • Neurology - Child Neurology

Academic Appointments

Honors and Awards

  • PERF-CNF 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)
  • Inductee, Arnold Gold Humanism Honor Society (2004)

Boards, Advisory Committees, Professional Organizations

  • Founding Member, ALD Connect (2014 - present)
  • Founding Member, The Global Leukodystrophy Initiative (GLIA) (2014 - present)

Professional Education

Board Certification: Neurology - Child Neurology, American Board of Psychiatry and Neurology (2010)
Post-doc: Stanford University Steinman & Robinson Labs, Neuroimmunology (2013)
Residency: Stanford University - Dept of Neurology CA (06/30/2010)
Residency: Massachusetts General Hospital MA (06/30/2007)
Internship: Massachusetts General Hospital MA (06/30/2006)
Medical Education: University of Rochester School of Medicine NY (2005)

Research & Scholarship

Current Research and Scholarly Interests

Our research group is dedicated to improving care for children with degenerative neurological disorders. We are particularly focused on genetic and autoimmune disorders that cause damage to the myelin (the fatty insulation around the nerves) of the brain and spinal cord. X-linked adrenoleukodystrophy (genetic) and multiple sclerosis (autoimmune) are the prototypical examples of degenerative disorders of myelin; these are the two disorders we study most intensively.

Our group has two primary areas of interest:

1. In the laboratory, we are hard at work developing diagnostic and therapeutic biomarkers for multiple sclerosis (MS) and X-linked adrenoleukodystrophy (ALD)

2. In the clinic, we are leading efforts to develop innovative care strategies for patients with demyelinating disorders.

One of the great obstacles to understanding and treating MS is its pathological heterogeneity. MS is currently defined solely by clinical and radiological criteria. Although these criteria have improved over time, abundant evidence suggests that pathophysiologic "subtypes" of MS still exist and, moreover, are indistinguishable from one another using current diagnostic criteria. Because potential differences in MS pathogenesis may result in divergent responses to the same treatment, this pathogenic variability poses serious hurdles to developing and implementing treatment strategies for affected patients.

The inflammatory cerebral demyelination of ALD represents a potential genetic model for MS. ALD is a monogenetic, X-linked disorder involving a gene (ABCD1) that encodes a peroxisomal protein. The incidence is ~1:17,000. The biochemical hallmark of the disease is an accumulation of very-long chain fatty acids in several tissues, including myelin and blood. Cerebral demyelination occurs in only a subset of patients, but is not related to genotype, suggesting a role for environmental modifiers, much like MS.

Our group is on the verge of exciting breakthroughs with the potential to shed important insight on the pathogenic and therapeutic pathways common to both MS and ALD. We hope to move these insights into clinical trials in the very near future.

We are proud to partner with disease consortiums and patient advocacy groups from around the world in the fight against these diseases.



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