Brandon L. Pearson

Brandon L. Pearson

Research Interest

Brief Summary of Research

Brandon Pearson studies genetic and environmental contributors to risk for developmental and aging associated disorders. His lab is currently focused on identifying origins of somatic mosaic mutation in the brain and the role of environmental exposures in trinucleotide repeat disorders such as Huntington’s disease. To this end, his lab uses cellular models, mice, and a short-lived fish species with sporadic neurodegeneration, the African Turquoise Killifish.

"My lab studies molecular and cellular mechanisms of developmental, psychiatric, and aging-associated disorders. Our overarching goal is to identify causal environmental and genetic factors. My research is inspired by 1) our exceptionally poor understanding of brain - behavior relationships in disease alongside 2) the enormous psychosocial, medical, and economic burdens of chronic brain and aging-associated diseases. My group searches for etiologies and mechanisms by leveraging a wide array of experimental and observational systems. We apply computational approaches, tissue culture, animal models (mice and fish), and human biospecimens. Our ultimate goal is to identify key molecular initiators of pathology in order to reveal viable opportunities for primary prevention– particularly for conditions that are sporadic and/or have a long latent progression. A current focus is determining how (and which) environmental exposures during developmental periods program molecular signatures involved in complex disease outcomes including autism spectrum disorder, Huntington’s disease, and brain aging."

Xie K*, Ryan DP*, Pearson BL*, Henzel KS, Neff F, Vidal RO, Hennion M, Lehmann I, Schleif M, Schröder S, Adler T, Rathkolb B, Rozman J, Schütz A, Prehn C, Edvar M, Weiergräber M, Adamski J, Busch DH, Ehninger G, Matynia A, Jackson WS, Wolf E, Fuchs H, Gailus-Durner V, Bonn S, Hrabe de Angelis M, Ehninger D. (2018). Epigenetic alterations in longevity regulators, reduced lifespan, and exacerbated aging-related pathology in old father offspring mice. Proceedings of the National Academy of Sciences USA 115(10):E2348-E2357. *Equal contribution

Ryan DP, Henzel KS, Pearson BL, Siwek ME, Papazoglou A, Paesler K, Müller R, Xie K, Schröder S, Becker L, Garrett L, Hölter SM, Neff F, Racz I, Rathkolb B, Rozman J, Ehninger G, Klingenspor M, Klopstock T, Wolf E, Wurst W, Zimmer A, Fuch H, Guilus-Durner V, Hrabe de Angelis M, Sidiropoulou K, M Weiergräber M, Ehninger D (2018). A paternal methyl donor-rich diet altered cognitive and neural functions in offspring mice. Molecular Psychiatry 23(5): 1345-1355.

Pearson BL*, Simon JM*, McCoy ES, Salazar G, Fragola G, Zylka MJ (2016). Identification of chemicals that mimic transcriptional changes associated with autism, brain aging and neurodegeneration. Nature Communications 7:11173. *Equal contribution

King IF, Yandava CN, Mabb AM, Hsiao JS, Huang H, Pearson BL, Calabrese JM, Starmer J, Parker JS, Magnuson T, Chamberlain SJ, Philpot BD, Zylka MJ. (2013). Topoisomerases facilitate transcription of long genes linked to autism. Nature 501: 58-62

Pearson BL, Defensor EB, Pobbe RLH, Yamamoto L, Bolivar VJ, Blanchard DC, Blanchard RJ (2012). MeCP2 truncation in male mice promotes affiliative social behavior. Behavior Genetics 42: 299-312

Sugawara A*, Pearson BL*, Blanchard DC, Ward MA (2012). Mouse females devoid of exposure to males during fetal development exhibit increased maternal behavior. Psychoneuroendocrinology 37(3): 383-395.  * Equal contribution

Pearson BL, Pobbe RLH, Defensor EB, Oasay L, Bolivar VJ, Blanchard DC, Blanchard RJ (2011). Motor and cognitive stereotypies in the BTBR T+tf/J mouse model of autism. Genes, Brain and Behavior 10, 228-235.

For a complete list of publications visit 

https://www.ncbi.nlm.nih.gov/myncbi/brandon.pearson.1/bibliography/public/

 

 

 

  • BS, 2005 University of New Mexico
  • MS, 2007 Bucknell University
  • PhD, 2012 University of Hawaii
  • Postdoc, 2015 University of North Carolina at Chapel Hill
  • Postdoc, 2017 German Center for Neurodegenerative Diseases
  • Neurodevelopmental Toxicity 
  • Developmental Origins of Health and Disease 
  • Mutagenesis 
  • Neural Degeneration and Repair 
  • Columbia University CIMER Mentor Training