Markus Riessland

Markus Riessland

 

 

Markus Riessland, PhD

Assistant Professor, Empire Innovation Program (Aging Brain)
Department of Neurobiology and Behavior
 
Markus.Riessland@stonybrook.edu

CMM Room 536
Phone (631) 632-4801

 


Open positions in the lab:
Postdoctoral Associate
Research Support Specialist


Markus Riessland is a trained molecular biologist with a background in neuroscience, human genetics and neurodegenerative diseases. Early in his career, Dr. Riessland was involved in several internationally funded projects, where he performed and published studies on epigenetic modifiers as a potential therapy for the neurodegenerative disease spinal muscular atrophy (SMA). His research is particularly focused on the identification and characterization of neuron-specific disease-modifying factors that may facilitate the development of novel therapeutic strategies for degenerative disorders of the central nervous system.

Dr. Riessland focuses on the understanding of cellular senescence. Cellular senescence is a common biological process in which mitotic cells may shut down cell cycle when they recognize they have suffered DNA damage during division This process causes the generation of “undead cells” (a.k.a. Zombie Cells). This helps to prevent damaged cells from growing uncontrollably and causing problems like cancer. Undead cells are, in fact, pretty common and they are found all over the body.

However, senescence is not typically seen in the nerve cells of the brain. Unlike most other cells in the body, neurons stop dividing once they’re fully formed. Dr. Riessland discovered that, surprisingly, post-mitotic dopaminergic neurons —which regulate motivation, memory, and movement by producing chemical messenger dopamine—can nevertheless become senescent. This finding could have widespread implications for the understanding of many age-related neurodegenerative disorders (e.g. Parkinson’s disease) and the aging process itself.

Currently, his lab uses stem cell-based approaches as well as mouse models and next generation sequencing techniques (TRAP-seq, RNA-seq, ATAC-seq, scRNA-seq etc.) to tackle the questions where and how cellular senescence in the brain can occur and spread, which cell types are involved and what the molecular triggers are. Additionally, research in the lab focuses on the identification and molecular characterization of genetic modifiers that influence the vulnerability of neuronal subtypes. The knowledge of molecular modifiers helps to understand the underlying reasons of vulnerability which could be leveraged to protect cells from neurodegeneration. Moreover, the lab’s research aims to interfere with the aging process by ameliorating the unwanted negative effects of cellular senescence. Dr. Riessland received his PhD from the Clinic of the University Cologne, Institute for Human Genetics, Germany.

  • Publications
  •  
    • Riessland M. (2020). Is Cellular Senescence of Dopaminergic Neurons the Cause of Local Inflammation in the Midbrain Observed in Parkinson’s Disease? J Cell Immunol.; 2(5): 201-204. (Invited Commentary)
       
    • Riessland, M. (2019). Is there hope for spinal muscular atrophy synthetic pharmacotherapy? Expert Opin Pharmacother, 1-4. (Invited Review)
    • Riessland, M.*, Kolisnyk, B., Kim, T.W., Cheng, J., Ni, J., Pearson, J.A., Park, E.J., Dam, K., Acehan, D., Ramos-Espiritu, L.S., et al. (2019). Loss of SATB1 Induces p21-Dependent Cellular Senescence in Post-mitotic Dopaminergic Neurons, Cell Stem Cell, https://doi.org/10.1016/j.stem.2019.08.013 (*Lead Contact)
    • Riessland, M., Kolisnyk, B., and Greengard, P. (2017). Reactive Dopamine Leads to Triple Trouble in Nigral Neurons. Biochemistry 56, 6409-6410.
    • Eacker, S. M., K. Crawford, L. Brichta, M. Riessland, N. T. Ingolia, P. Greengard, T. M. Dawson and V. L. Dawson (2017). Experience-dependent translational state defined by cell type-specific ribosome profiling bioRxiv. 169425; doi: https://doi.org/10.1101/169425
    • Riessland, M., A. Kaczmarek, S. Schneider, K. J. Swoboda, H. Lohr, C. Bradler, V. Grysko, M. Dimitriadi, S. Hosseinibarkooie, L. Torres-Benito, M. Peters, A. Upadhyay, N. Biglari, S. Krober, I. Holker, L. Garbes, C. Gilissen, A. Hoischen, G. Nurnberg, P. Nurnberg, M. Walter, F. Rigo, C. F. Bennett, M. J. Kye, A. C. Hart, M. Hammerschmidt, P. Kloppenburg and B. Wirth (2017) Neurocalcin Delta Suppression Protects against Spinal Muscular Atrophy in Humans and across Species by Restoring Impaired Endocytosis Am J Hum Genet 100(2): 297-315.
      [highlighted in Editor’s Corner of AJHG, and rated “exceptional” on F1000]
    • Kaczmarek A, Schneider S, Wirth B, Riessland M* (2015) Investigational therapies for the treatment of spinal muscular atrophy. Expert Opin Investig Drugs 24: 867-81. doi: 10.1517/13543784.2015.1038341 (*Invited Review)
    • Wishart TM*, Mutsaers CA*, Riessland M*, Reimer MM*, Hunter G, Hannam ML, Eaton SL, Fuller HR, Roche SL, Somers E, Morse R, Young PJ, Lamont DJ, Hammerschmidt M, Joshi A, Hohenstein P, Morris GE, Parson SH, Skehel PA, Becker T, Robinson IM, Becker CG, Wirth B, Gillingwater TH (2014) Dysregulation of ubiquitin homeostasis and beta-catenin signaling promote spinal muscular atrophy. J Clin Invest 124: 1821-34. doi: 10.1172/JCI71318 (*equal contribution)
    • van Dijk FS*, Zillikens MC*, Micha D*, Riessland M*, Marcelis CL, de Die-Smulders CE, Milbradt J, Franken AA, Harsevoort AJ, Lichtenbelt KD, Pruijs HE, Rubio-Gozalbo ME, Zwertbroek R, Moutaouakil Y, Egthuijsen J, Hammerschmidt M, Bijman R, Semeins CM, Bakker AD, Everts V, Klein-Nulend J, Campos-Obando N, Hofman A, te Meerman GJ, Verkerk AJ, Uitterlinden AG, Maugeri A, Sistermans EA, Waisfisz Q, Meijers-Heijboer H, Wirth B, Simon ME, Pals G (2013) PLS3 mutations in X-linked osteoporosis with fractures. N Engl J Med 369: 1529-36. doi: 10.1056/NEJMoa1308223 (*equal contribution)
    • Somers E*, Riessland M*, Schreml J, Wirth B, Gillingwater TH, Parson SH (2013) Increasing SMN levels using the histone deacetylase inhibitor SAHA ameliorates defects in skeletal muscle microvasculature in a mouse model of severe spinal muscular atrophy. Neurosci Lett 544: 100-4. doi: 10.1016/j.neulet.2013.03.052 (*equal contribution)
    • Riessland M, Ackermann B, Forster A, Jakubik M, Hauke J, Garbes L, Fritzsche I, Mende Y, Blumcke I, Hahnen E, Wirth B (2010) SAHA ameliorates the SMA phenotype in two mouse models for spinal muscular atrophy. Hum Mol Genet 19: 1492-506