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Annelise E. Barron

Academic Appointments

  • Associate Professor of Bioengineering

Key Documents

Contact Information

  • Academic Offices
    Personal Information
    Alternate Contact
    Raul Felipa Finance Administrator, Stanford Dept. of Bioengineering Tel Work 650-725-7665


Current research: Molecular and cellular biophysics of human innate immunity, with a focus on the pleiotropic roles of host defense peptides and amyloidogenic peptides in human health and disease.

Previous research: Design, synthesis, and biophysical studies of sequence-controlled, biomimetic oligomers (synthetic peptide mimics) with helical structures, for biomedical and biomaterial applications (mimicry of lung surfactant proteins and antimicrobial peptides). Also in previous work: design and synthesis of novel polymeric materials and strategies for capillary and microchip electrophoresis (DNA sequencing and genotyping); polymer-biomolecule conjugates.

Academic Appointments

Administrative Appointments

  • Associate Chair for Graduate Studies, Department of Bioengineering (2010 - 2015)

Honors and Awards

  • Nanobio Scholar, Virginia Tech (2011)
  • W.M. Keck Associate Professor of Bioengineering, Stanford University (2007-present)
  • Thiele Lecturer in Chemical Engineering, University of Notre Dame (2005)
  • Camille Dreyfus Teacher-Scholar Award, Camille and Henry Dreyfus Foundation (2002)
  • DuPont Young Professor Award, DuPont, Inc. (2002)
  • Presidential Early Career Award for Scientists and Engineers, NIH/NHGRI (1999)
View All 19honors and awards of Annelise Barron

Professional Education

Postdoc: UCSF/Chiron Corporation, Biomimetic & Bioorganic Chemistry (1997)
Postdoc: Soane BioSciences/ACLARA Biosciences Inc., Molecular Biotechnology (1996)
Ph.D.: Univ. of California, Berkeley, Chemical Engineering (1995)
B.S.: Univ. of Washington, Seattle, Chemical Engineering (1990)

Research & Scholarship

Current Research and Scholarly Interests

According to our recent findings, dysfunctional innate immune responses in humans and other mammals involving infection-, injury-, or stress-related dynamic imbalances between particular, potently cytotoxic host defense peptides we study, and pro-amyloid / fibrillogenic peptides including ABeta and IAPP, may play a role in the poorly understood etiology of chronic / progressive plaque diseases, including psoriasis, lupus erythematosus, diabetes type II melittus, atherosclerosis, and particularly, Alzheimer's Disease. All of these diseases involve inflammation and plaque accumulation.

The latter disease, Alzheimer's, is in need of a major breakthrough in fundamental understanding, more than almost any human disease currently under study. Of a total of 244 clinical trial initiated by big pharma towards the development of anti-Alzheimer's drugs, 243, or 99.7% of these trials have failed utterly. There is no current treatment. Obviously, the most fundamental ideas for what drives Alzheimer's are flawed.

Moreover, until recently Alzheimer's disease was believed to be the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention (CDC). But in March 2014, new research published in Neurology suggested that Alzheimer’s may actually be responsible for as many deaths each year as heart disease or cancer – the two leading causes of death in the U.S. – due to issues, in hospitals, of improper prior determinations of underlying cause of death in the elderly.

My lab is testing novel mechanistic hypotheses of Alzheimer's etiology, based on recent, unique molecular biophysical observations of pro-amyloid and innate immune peptides.

Increasing numbers of epidemiological and co-morbidity studies indicate that multiple, progressive degenerative diseases, all involving plaque deposition in various body compartments, are linked. For instance, many researchers have begun to refer to Alzheimer's Disease as "Diabetes Melittus Type III". We seek, with current projects, to sleuth out the shared molecular biophysical bases for these emerging linkages.

(Note: Succinct, exemplary summaries of these fascinating epidemiological / comorbidity linkages are found, for instance, in the following papers: "The ‘psoriatic march’: a concept of how severe psoriasis may drive cardiovascular comorbidity", 2011 John Wiley & Sons A/S, Experimental Dermatology, 20, 303–307; "Circle of Willis atherosclerosis: association with Alzheimer’s disease, neuritic plaques and neurofibrillary tangles", Acta Neuropathol (2007) 113:13–21; "Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis", Arch Dermatol Res (2006) 298:321–328; "Association of Alzheimer disease pathology with abnormal lipid metabolism", Neurology 2011;77;1068).




Prior Year Coursescourses of Annelise Barron



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