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Detlev Boison, PhD

Detlev Boison, PhD

Robert S. Dow Chair of Neurology & Director of Neurobiology Research
Director of Basic and Translational Research, Legacy Research Institute
Adjunct Professor, Dept. of Neurology, OHSU
Adjunct Professor, Dept. of Neuroscience, Washington State University

Contact Info:

Telephone: 503-413-1754 | Fax: 503-413-5465  |  Email: dboison@downeurobiology.org

Links:

CV (updated Dec 2017) 
Peer reviewed publications
R. S. Dow Neurobiology Laboratories
OHSU faculty profile  |  WSU faculty profile

Short Bio:

Having a passion for translational research and for finding cures for intractable conditions that cause human suffering and death, I seek to translate fundamental mechanisms of biochemistry and energy homeostasis into novel therapeutic approaches for the treatment of neurological conditions and cancer. A major research effort is the development of therapies that restore the equilibrium of adenosine and thereby reset the ‘disease clock’.

I graduated at the University of Köln, Germany, in 1994 with a PhD in Biochemistry. In 1995 I started my independent research career at the University and Federal Institute of Technology in Zürich where I received the venia legendi in Cellular Pharmacology in 2005 for my work on cell-based adenosine augmentation therapies for epilepsy.

That same year I joined Legacy Health in Portland, Oregon, where I am currently Chair and Director of the Robert Stone Dow Neurobiology Laboratories and Director of Basic and Translational Research of the Legacy Research Institute. In addition, I hold faculty appointments at Oregon Health and Science University and at Washington State University. I have published over 140 papers with an h-index of 45 and have delivered over 120 lectures in more than 20 different countries.

Publication Highlights:

Regulation of Endothelial Intracellular Adenosine via Adenosine Kinase Epigenetically Modulates Vascular Inflammation.
Xu Y, Wang Y, Yan S, Yang Q, Zhou Y, Zeng X, Liu Z, An X, Dong Z; Jiang X, Fulton DJ, Neal L, Weintraub NL, Li Q, Bagi Z, Hong M, Boison D, Wu C; Huo Y.
Nature Communications. 2017, 16;8(1):943.
https://www.ncbi.nlm.nih.gov/pubmed/29038540

Epigenetic changes induced by adenosine augmentation therapy prevent epileptogenesis.
Williams-Karnesky RL, Sandau US, Lusardi TA, Lytle NK, Farrell JM, Pritchard EM, Kaplan DL, Boison D
Journal of Clinical Investigation. 2013, 123(8):3552-3563.
https://www.ncbi.nlm.nih.gov/pubmed/23863710

Adenosine augmentation ameliorates psychotic and cognitive endophenotypes of schizophrenia in mice.
Shen H-Y, Singer P, Lytle N, Wei C, Lan J-Q, Williams-Karnesky RL, Chen J-F, Yee BK, Boison D
Journal of Clinical Investigation. 2012, 122(7):2567-2577
https://www.ncbi.nlm.nih.gov/pubmed/22706302

A ketogenic diet suppresses seizures in mice through adenosine A1 receptors.
Masino SA, Li T, Theofilas P, Sandau US, Ruskin DN, Fredholm BB, Geiger JD, Aronica E, Boison D
Journal of Clinical Investigation. 2011, 121(7):2679-83.
https://www.ncbi.nlm.nih.gov/pubmed/21701065

Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice.
Li T, Ren G, Lusardi T, Wilz A, Lan JQ, Iwasato T, Itohara S, Simon RP, Boison D.
Journal of Clinical Investigation. 2008, 118(2):571-582.
https://www.ncbi.nlm.nih.gov/pubmed/18172552

Research Interests:

  • The biochemistry and epigenetics of epilepsy
  • Focal adenosine-augmentation therapies to treat epilepsy
  • Therapies for epilepsy prevention
  • Brain regeneration after traumatic brain injury and stroke
  • Comorbidities in Neurology
  • The adenosine hypothesis of schizophrenia
  • Role of adenosine in cancer
  • Metabolic therapies

Research Focus:

Detlev Boison has a passion for translational research and finding cures for intractable conditions that cause human suffering and death. He incorporates insights from the evolution of life in his research design with the goal to treat the underlying causes of disease and not just the symptoms. One of his greatest passions has been his work with adenosine and finding therapies that can help reset the equilibrium of energy homeostasis. Having been part of the ‘primordial soup’ of our early planet, adenosine played an important role in the origin of life. It is not only part of ATP, representing energy, but also of RNA, reflecting metabolic activities. Therefore, adenosine evolved as a critical bioenergetic regulator. Under conditions of energy or oxygen deprivation (e.g. a stroke, or within the hypoxic environment of a cancer) or excessive energy consumption (e.g. during an epileptic seizure) adenosine levels rapidly rise and serve the function to restore equilibrium and to promote energy supply (e.g. through angiogenesis) or to suppress energy consuming processes (e.g. stop a seizure). Not surprisingly, we found disruption of adenosine homeostasis in a wide range of pathologies including epilepsy, stroke, traumatic brain injury, Alzheimer’s disease, Parkinson’s disease, schizophrenia, and cancer.

A major focus of Dr. Boison’s work is the adenosine regulating enzyme adenosine kinase (ADK), which in the adult brain is primarily expressed in astrocytes, which control the environment in which neurons thrive and survive. Pathological overexpression of ADK results in adenosine deficiency, which in turn promotes epileptic seizures, sleep dysfunction, cognitive impairment, psychiatric symptoms, and lack of dopamine responses. Consequently, adenosine augmentation therapies are a rationale therapeutic approach to restore equilibrium in a wide range of neurological conditions. To avoid side effects of systemic adenosine augmentation, focal adenosine augmentation therapies have been developed. A major focus is the development of adenosine releasing polymeric or cell-based brain implants and the development of adenosine augmenting gene therapies. Metabolic interventions, such as a high fat low carbohydrate ketogenic diet, likewise enhance adenosine signaling in the brain. A new line of research involves a specific role of the nuclear isoform ADK-L as epigenetic regulator. By removing adenosine ADK-L drives the flux of methyl groups through the transmethylation pathway resulting in increased global DNA and histone methylation. Those maladaptive epigenetic alterations play a major role in disease development and progression. Consequently, targeting the epigenetic mechanisms of adenosine provides a unique strategy to prevent the development and progression of epilepsy.