Ferenc Deak, MD, PhD

Assistant Professor, Donald W. Reynolds Oklahoma Center on Aging


University of Oklahoma Health Sciences Center
975 NE 10th Street
SLY-BRC 1309-B
Oklahoma City, OK 73104
(405) 271-8000 ext. 47817


1994            M.D., Semmelweis University, Budapest, Hungary
2000            Ph.D., Semmelweis University, Budapest, Hungary
2000-2008   Post-doctoral fellowship at UT Southwestern (supported by HHMI)

Research Interests

The neurophysiological laboratory is the latest addition to the Reynolds Oklahoma Center on Aging at the University of Oklahoma Health Sciences Center in Oklahoma City, OK. Research in Dr. Deák's laboratory is focused on synaptic communication among neurons in the aging brain with an emphasis on molecular regulation of neurotransmission and its defects in dementia.

  • Synaptic neurotransmission
  • Neuronal dysfunction in Aging
  • Mild Cognitive Impairment
  • Vascular Cognitive Impairment
  • Epilepsy and Aging

We combine a large range of techniques from the molecular to the system level to understand the information processing and memory function of the nervous system. We synthesize this knowledge with the medical observations about aging’s effect on the brain in general and specifically about Alzheimer's, Parkinson's, and other neurodegenerative diseases. Our aim is to reveal the pathophysiology and to achieve progress in early diagnosis and effective treatment for these devastating diseases.

Active areas of research include:

  1. Neuronal communication: The permanent focus of our laboratory is the molecular mechanism of synaptic neurotransmitter release and plasticity, the crucial element for information processing and the higher human cognitive functions, such as abstract thinking and moral conduct.

  2. Cognitive decline and Neurodegenerative disorders: We utilize genetically engineered mouse models to study synaptic changes in early stage of different neurodegenerative diseases, with special interest paid to Alzheimer's and Parkinson's diseases.

  3. Molecular mechanisms in Epilepsy and Dementia: We build in vitro models to clarify the mechanism how specific mutations cause epileptic seizures and dementia. Our laboratory is able to test small molecular compounds with putative therapeutic effect in these diseases.

To achieve the listed aims specific state-of-the-art methods are applied in the laboratory, including molecular biology and biochemistry; primary neuronal cultures and slices from transgenic mice; fluorescence imaging of synaptic vesicle fusion and endocytosis and electrophysiology. We perform extracellular recording of long-term synaptic plasticity in hippocampal slices and intracellular patch clamp recordings from cultured cells. The scope of our experiments spans from single quantal release events (miniature synaptic potentials) to analysis of neuronal network activity. We extensively study the regulation of short-term synaptic plasticity (depression and facilitation).

Service to the University and the Scientific Community

Dr. Deák is active in teaching multiple topics in human physiology, molecular neuroscience and healthy aging of the brain. He has mentored many students and post-doctoral fellows, introduced them to the cutting edge scientific methods used in the laboratory and helped them starting their own carrier.

Dr. Deák has published dozens of original manuscripts and invited reviews in top ranking journals, served as reviewer of PNAS, J Neuroscience and other scientific periodicals as well as various grant funding agencies. Dr. Deák has been invited to present his research at national and international meetings and results from his research have been cited frequently.

Most Relevant and Recent Publications

  1. Deák F, Sonntag WE.  Aging, Synaptic Dysfunction, and Insulin-Like Growth Factor (IGF)-1. J Gerontol A Biol Sci Med Sci. 2012 67:611-25. PMID: 22503992. PMCID: PMC3348499.

  2. Deák F, Schoch S, Liu X, Südhof TC, Kavalali ET.  Synaptobrevin is essential for fast synaptic-vesicle endocytosis.  Nat Cell Biol. 2004 Nov;6(11):1102-8. Epub 2004 Oct 10. PMID: 15475946.

  3. Schoch S*, Deák F *, Konigstorfer A*, Mozhayeva M, Sara Y, Sudhof TC, Kavalali ET.  SNARE function analyzed in synaptobrevin/VAMP knockout mice.  Science 2001 Nov 2; 294(5544):1117-22.  PMID:11691998. *Equal contribution

  4. Deák F, Shin O, Kavalali ET, Südhof TC.  Structural determinants of synaptobrevin 2 function in synaptic vesicle fusion.  J Neurosci. 2006 Jun 21;26(25):6668-76. PMID: 16793874.

  5. Sara Y*, Virmani T*, Deák F, Liu X, Kavalali ET.  An isolated pool of vesicles recycles at rest and drives spontaneous neurotransmission.  Neuron. 2005 Feb 17;45(4):563-73. PMID: 15721242.

  6. Deák F*, Xu Y*, Chang W, Dulubova I, Khvotchev M, Liu X, Südhof TC, Rizo J.  Munc18-1 Binding to the Neuronal SNARE Complex Controls Synaptic Vesicle Priming.  J Cell Biol. 2009 Mar 9;184(5):751-64. Epub 2009 Mar 2. PMID: 19255244. PMCID: PMC2686405.

  7. Deák F, Shin O, Tang J, Hanson P, Ubach J, Jahn R, Rizo J, Kavalali ET, Südhof TC.  Rabphilin regulates SNARE-dependent re-priming of synaptic vesicles for fusion.  EMBO J. 2006 Jun 21;25(12):2856-66. Epub 2006 Jun 8. PMID: 16763567

  8. Deák F, Lasztóczi B, Pacher P, Petheő G, Kecskeméti V, Spät A. Inhibition of voltage-gated calcium channels by fluoxetine in rat hippocampal pyramidal cells.  Neuropharmacology. 2000 Apr 3;39(6):1029-36. PMID: 10727713.

  9. Deák F, Nagy G, Várnai P, Madarász E, Spät A. Calcium current activated by potassium ions in voltage-clamped rat hippocampal pyramidal neurons.  J Physiol. 1998 May 1;508 ( Pt 3):735-45. PMID: 9518729. PMCID: PMC2230920.

  10. Deák F, Liu X, Khvotchev M, Li G, Kavalali ET, Sugita S, Südhof TC.  Alpha-latrotoxin stimulates a novel pathway of Ca2+-dependent synaptic exocytosis independent of the classical synaptic fusion machinery.  J Neurosci 2009 Jul 8; 29(27):8639-48.  PMID:19587270. PMCID:2739239. NIHMS:133617.