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Bogdan                         Beirowski

Bogdan K. Beirowski MD, PhD

Department of Biochemistry

Assistant Professor
Principal Investigator at the Hunter James Kelly Research Institute

Specialty/Research Focus

Apoptosis and cell death; Bioinformatics; Molecular and Cellular Biology; Molecular Basis of Disease; Molecular genetics; Neurobiology; Regulation of metabolism

 
Professional Summary:

My laboratory studies the cell-autonomous and non-cell-autonomous mechanisms of axon degeneration, a process akin to programmed cell death. In other words, we are attempting to elucidate what causes axon breakdown from within neurons and which external (glial) events trigger axon loss. Degeneration of axons is a hallmark in many neurodegenerative conditions, including those associated with abnormal glia. We have great hope that understanding why and how axons degenerate may lead to more efficient neuroprotective therapies tailored specifically to support axons and their surrounding glia.

Axons are the longest cellular projections of neurons relaying electrical and biochemical signals in nerves and white-matter tracts of the nervous system. As such, they are critical for neuronal wiring and transport of neuronal maintenance signals. Because of their incredible length and energetic demand (human motor neurons can be one meter long), however, axons are very vulnerable and at continuous risk of damage. Axons do not exist in isolation but are inextricably and intimately associated with their enwrapping glia (Schwann cells and oligodendrocytes) to form a unique axon-glia unit.

The most relevant neurological symptoms in a number of debilitating neurodegenerative conditions are due to compromised axon integrity. Thus, neuroprotective therapies promoting axon stability have great potential for more effective treatment. Recent studies indicate that axonal degeneration, at least in experimental settings, is an active and highly regulated process akin to programmed cell death (‘axonal auto-destruction’). Moreover, it is increasingly realized that axonal maintenance relies not only on neuron-derived provisions but also on trophic support from their enwrapping glia. The mechanism for this non-cell-autonomous support function remains unknown, but emerging evidence indicates that it is distinct from the glial role in insulating axons with myelin.

We are pursuing the intriguing question of whether abolished support by aberrant delivery of metabolites and other trophic factors from glia into axons is mechanistically linked to the induction of axonal auto-destruction. This concept is supported by our recent finding that metabolic dysregulation exclusively in Schwann cells is sufficient to trigger axon breakdown.

Education and Training:
  • PhD, Molecular Biology, University of Cambridge (2010)
  • Dr. med., Medicine, University of Cologne (2005)
Employment:
  • Assistant Professor, Department of Biochemistry, Hunter James Kelly Research Institute (2016-present)
  • Post Doctoral Fellow, Department of Genetics, Washington University School of Medicine (2010–2016)

Grants and Sponsored Research:
  • August 2012–July 2015
    Modeling Axon Loss in CMT by Disruption of Schwann Cell Metabolic Regulation
    Muscular Dystrophy Association
    Role: Principal Investigator
    $180,000

Journal Articles:
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School News:
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Contact Information

Hunter James Kelly Research Institute
NYS Center Of Excellence in Bioinformatics & Life Sciences
B4-314
Buffalo, NY 14203
Phone: (716) 888-4883
Email: bogdanbe@buffalo.edu


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