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Annelise E. Barron is the W.M. Keck Associate Professor of Bioengineering at Stanford University. The broad theme of the Barron lab is the study and biomimicry of natural host defense peptides (antimicrobial peptides). We study the molecular biophysics and mechanisms of LL-37—a centrally important human host defense peptide—and its involvement in Alzheimer's dementia (via LL-37 dysregulation and degradation by pathogen virulence factors). Alzheimer's dementia can be caused by (or at least, accompanied by) cerebral infections, a phenomenon now receiving renewed attention given recent discoveries. We are also working to develop biostable peptoid mimics of LL-37 as therapeutics that can combat antibiotic-resistant infections. Finally, we are working to mimic lung surfactant proteins that facilitate the delivery of therapeutics to the lungs, treat bacterial and viral pneumonia, or prevent or treat ventilator-associated acute lung injury. We are currently putting efforts into better understanding the pathogenic mechanisms of Covid-19, as relates to dysregulation of innate immunity; understanding why certain minority populations seem to be more strongly affected by Covid-19 infections; and developing therapeutic approaches to both preventing and treating severe Covid-19.Dr. Barron was trained as a chemical engineer at the University of Washington (B.S.) and U.C. Berkeley (Ph.D., under the mentorship of Prof. Harvey W. Blanch), and was a Pharmaceutical Chemistry postdoc with Prof. Ken A. Dill (UCSF) and Dr. Ronald N. Zuckermann (Chiron Corp.). She has served on the faculty at Stanford since 2007, and prior to that, served on the Chemical & Biological Engineering faculty of Northwestern University in Evanston, IL for 10 years (1997-2007). Dr. Barron has been awarded the NIH Pioneer Award (2020), the Presidential Early Career Award for Scientists & Engineers (PECASE) through NIH / NHGRI (1999), the Beckman Young Investigator Award (1999), and the Camille Dreyfus Teacher-Scholar Award (1998), among other awards. Dr. Barron was the youngest scientist ever to serve on the Scientific Advisory Committee to the Director of the NIH, under Dr. Elias Zerhouni. She has more than 175 publications and a current H-index of 52 (Web of Science, All Databases), and serves on the advisory boards of several biotechnology companies. She is proud to be 1/4 Quechua (the Native American people of Bolivia), 1/4 Hispanic, 1/4 Swedish, 1/4 English, and 100% American.
According to our recent findings and those of others, innate immune responses in humans and other mammals involving infection-, injury-, or stress-related dynamic imbalances between particular, immunomodulatory 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 diabetes type II melittus, atherosclerosis and Alzheimers dementia. All of these diseases involve dysbiosis, senescent/dystrophic cells, inflammation, and proteopathies with plaque accumulation; and can be complicated by infection.The latter disease, Alzheimers dementia, is in need of a major breakthrough in fundamental understanding, more than almost any human disease currently under study. Of a total of 430+ clinical trials initiated by Pharma towards the development of Alzheimer's treatments over the past 16+ years, all of these trials have failed (save one in 2021: Biogen's Aduhelm, which provides little if any patient benefit, is not covered by Medicare unless patients are in a clinical trial, and is not approved by the European Medicines Agency for use in the EU). There is no current effective pharmaceutical treatment for dementia. Obviously, the most fundamental ideas for what drives Alzheimers must be flawed or incomplete.Until recently Alzheimers 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 Alzheimers 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 Alzheimers etiology, based on recent, unique molecular biophysical observations of pro-amyloid and innate immune peptides. We are also looking at linkages to certain chronic infections and innate immune dysregulation.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, some researchers have begun to refer to Alzheimers Disease as "Diabetes Melittus Type III". We seek, with current research projects, to sleuth out the shared molecular biophysical and physiological bases for these emerging linkages, so that these conditions may be prevented.(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", Experimental Dermatology (2011) 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).