Current Research Interests:
Genes Involved in Behavior, Neurological, and Psychiatric Disorders
We are interested in finding and functionally characterizing genes involved in neurological disorders including deafness and ataxia and in behavioral and psychiatric diseases. In contrast to Mendelian single gene defects, human behavior and risk for psychiatric illness such as depression and alcoholism are determined by a complex interaction of environmental and multiple genetic risk factors. With the Human Genome sequenced, unprecedented numbers of genetic variants identified, and novel technologies that allow the study of genetic variants, untangling these risk factors is now possible. Once identified, we investigate the functional effects of the genetic variants, and the encoded proteins in vitro and in model organisms in order to better understand behavioral and neurological disorders.
Specifically, we are interested in identifying genetic risk factors for bipolar disorder and for addiction. In our studies, we also search for genetic variants that influence traits related to psychiatric disorders: For example, high scores on the personality domain "neuroticism" are indicative of increased risk for depression, and high impulsivity and low executive function are risk factor for addiction.
The genome project allowed large scale genetic studies, but also genome-wide studies of function, as in gene expression microarrays and proteomics. By combining genetic with functional studies, we identify genes involved in rare Mendelian disorders (deafness and ataxia), and are actively recruiting additional families with rare neurological disorders. We also predict that to untangle genetic risk factors for psychiatric disorders and addiction, such a combined approach will be useful. For these studies we use either cell lines from patient and control blood samples, or postmortem brains, and are currently testing whether fibroblasts can be induced to become neuronal using induced stem cells. While primarily interested in human disorders, we are using mice as a model system when appropriate. We use genetic methodologies and have identified specific single gene mutations that cause ataxia, seizures, and behavioral abnormalities in mice and humans. We collaborate with clinicians, psychologists, epidemiologists, statisticians and bioinformaticians as well as other geneticists in these endeavors.
- Co-Director, Bioinformatics graduate program, Center for Computational Medicine and Bioinformatics
- Faculty member of interdisciplinary graduate programs: Neuroscience, Cell & Molecular Biology.
- Diplom (Master) in Biochemistry, Free University of Berlin and Weizman Institute of Science, Rehovot, Israel.
- Ph.D., European Molecular Biology Laboratory (EMBL) and University of Heidelberg.
- Postdoctoral Fellow, University of California San Francisco.
Honors and Awards:
Distinguished Professor, Bio-X Center, Shanghai Jiao Tong University, China
Michael Weston Visiting Professorship, Weizmann Inst. of Science, Rehovot, Israel
Fellow of the "Studienstiftung des Deutschen Volkes" (German Phi Beta Kappa Equivalent).
Minerva (German Israeli Exchange) Fellowship.
Postdoctoral Fellowship from the German Academic Exchange Committee (DAAD).
NARSAD Distinguished Investigator Award 2008 and many earlier NARSAD awards
March of Dimes Basil O'Connor Starting Investigator Award.
Klingenstein Fellowship Award in the Neurosciences.
Alexander von Humboldt Foundation Fellowship for Sabbatical in Berlin, Germany.
Schoen CJ, Emery SB, Thorne MC, Ammana HR, Sliwerska E, Arnett J, Hortsch M, Hannan F, Burmeister M, Lesperance MM Increased activity of Diaphanous homolog 3 (DIAPH3)/diaphanous causes hearing defects in humans with auditory neuropathy and in Drosophila, Proc Natl Acad Sci U S A. 2010 Jul 12. [Epub ahead of print]
Wojnar M, Brower KJ, Strobbe S, Ilgen M, Matsumoto H, Nowosad I, Sliwerska E, Burmeister M. Association Between Val66Met Brain-Derived Neurotrophic Factor (BDNF) Gene Polymorphism and Post-Treatment Relapse in Alcohol Dependence. Alcohol Clin Exp Res 33: 693-702, 2009.
Zöllner S, Su G, Stewart WC, Chen Y, McInnis MG, Burmeister M: Bayesian EM algorithm for scoring polymorphic deletions from SNP data and application to a common CNV on 8q24. Genet. Epidemiology 33(4):357-68, 2009.
Scott LJ, Muglia P, Kong XQ, Guan W, Flickinger M, Upmanyu R, Tozzi F, Li JZ, Burmeister M, Absher D, Thompson RC, Francks C, Meng F, Antoniades A, Southwick AM, Schatzberg AF, Bunney WE, Barchas JD, Jones EG, Day R, Matthews K, McGuffin P, Strauss JS, Kennedy JL, Middleton L, Roses AD, Watson SJ, Vincent JB, Myers RM, Farmer AE, Akil H, Burns DK, Boehnke M. Genome-wide association and meta-analysis of bipolar disorder in individuals of European ancestry. Proc Natl Acad Sci U S A 106(18):7501-6, 2009.
Sen S, Burmeister M: Hardy-Weinberg Analysis of a Large Set of Published Association Studies Reveals Genotyping Error and a Deficit of Heterozygotes Across Multiple Loci – Human Genomics 3(1): 36-52, 2008.
Burmeister, M, McInnis, MG, and Zoellner S: Psychiatric Genetics – Progress Amid Controversy. Nature Reviews Genetics 9: 527-540, 2008.
Links to additional information about the work of Dr. Burmeister.
Department of Psychiatry, University of Michigan
Department of Human Genetics, University of Michigan
Bioinformatics Graduate Program
Figure 1: Multiple risk factors for depression
Depression is thought to be caused by a combination of genetic factors, early experiences and stressful life events. Instead of comparing depressed subjects and controls, research on the genetics of personality can get at genetic predisposition genes for depression even while studying a general population sample.
Figure 2: The critical regions of Cayman Ataxia and the
jittery mousemutation overlap.
Physical maps of human 19p13.3 and mouse chromosome 10 showing (blue arrows) the regions to which the disorders have been localized. The green bar indicates a map inversion we identified previously, whereas the red bar is the region of overlap. The enlarged region shows the genes in the overlap. Atcay is the gene identified as the jittery and Cayman ataxia gene in our studies (see paper by Bomar et al., Nature Genetics 2003)
Figure 3: Psychiatric disorders overlap and might be extremes of personality traits.
Genetic vulnerabilities for psychiatric disorders are shown as emerging from the extreme end of normal population variations of personality, illustrated as different background shades of mood, anxiety, cognitive processing and volition. Volition, which was introduced by Kraepelin155, combines the will or the drive to do something with energy and activity level. Genetic factors affecting levels of these underlying traits,
in interaction with additional genetic and environmental factors, can lead to psychiatric disorders — shown here are bipolar disorder, schizophrenia, depression and anxiety disorders — the symptoms and genetic risk factors of which are in part unique and in part overlapping. Psychosis and panic are pathological traits and are not a formal diagnostic category, but are associated with several psychiatric diagnoses. Because not all disorders can be covered in two dimensions, interactions and overlaps exist in many more dimensions than can be represented here (for example, depression and anxiety are also present in schizophrenia).