Attila Köfalvi
00351-304-502-916
akofalvi@uc.pt
Research Associate
Group at CNC
Education: 

Dr. Attila Köfalvi graduated as a functional and developmental biologist with specialization in neurobiology in 1999 at the Faculty of Sciences, Eötvös Loránd University, Budapest, Hungary. In November, 2004 obtained PhD summa cum laude, after carrying out 5 years of a joint PhD programme in Neurobiology at the Semmelweis Medical University, Budapest, Hungary, at the Institute of Experimental Medicine, Budapest as well at the Nathan Smith Kline Institute in Orangeburg, NY, USA. He holds Good Laboratory Practice certificate (2001) and Category "C" qualification for directing animal experiments from the Federation of European Laboratory Animal Science Associations (2009). He is a neurobiologist at the Center for Neuroscience and Cell Biology of Coimbra at the Faculty of Medicine of the University of Coimbra, Coimbra, Portugal since 2004. He currently holds the position of research associate, and is head of his research subgroup called "Laboratory of Neuromodulation and Metabolism". In 2009, he became a Young Investigator of the Network of European Neuroscience Institutes.
He is integrated in the network of Associate Laboratories of the Portuguese Science Foundation. He is also holding associate researcher position at the Institute for Interdisciplinary Research since 2010.

Afiliation: 

CNC

Area of Research: 

Brain glucose metabolism is tightly coupled to neural activity. My lab investigates how modulators of neural activity regulate cerebral energy metabolism. The neuromodulators we are currently interested in and show promising therapeutic potential are adenosine, endocannabinoids, glucocorticoids, serotonin and insulin-like peptides.
Why is this research important? All neurological and psychiatric disorders are linked with persistent changes in glucose metabolism in very specific regions in the human brain. 18F-deoxyglucose and functional MRI imaging help neurologists detect these alterations. These metabolic dysregulations often precede the loss of brain cells by years. Hence, understanding the selective early markers of brain disorders can help the physicians to categorize the illness and select the appropriate treatments as early as possible. Many times, early recognition of the disease and swift decision on the treatment make the difference. Hence, we also would like to know if the restoration of the impaired brain glucoregulation could improve the outcome of the given brain disease, or even, prevent the onset of it. We are studying basic signalling systems, both in vitro and in vivo in animal models with the future aim of re-testing the promising ideas in humans.

 

Research Summary: 
http://orcid.org/0000-0001-6910-9707
Selected Publications: 

Köfalvi A, Rodrigues RJ, Ledent C, Mackie K, Vizi ES, Cunha RA, Sperlágh B (2005) Involvement of cannabinoid receptors in the regulation of neurotransmitter release in the rodent striatum: a combined immunochemical and pharmacological analysis. The Journal of Neuroscience 25(11):2874–2884.

Matias I, Di Marzo V, Köfalvi A (2008) Endocannabinoids in energy homeostasis and metabolic disorders. In: Cannabinoids and the Brain. Springer-Verlag; ed. A. Köfalvi DOI10.1007/978-0-387-74349-3_14

Garção P, Szabó EC, Wopereis S, Castro AA, Tomé AR, Prediger RD, Cunha RA, Agostinho P, Köfalvi A (2013) Functional interaction between presynaptic α6β2-containing nicotinic and adenosine A2A receptors in the control of dopamine release in the rat striatum. British Journal of Pharmacology 169(7):1600-1611.

Ferreira SG, Gonçalves FQ, Marques JM, Tomé ÂR, Rodrigues RJ, Nunes-Correia I, Ledent C, Harkany T, Venance L, Cunha RA, Köfalvi A (2015) Presynaptic adenosine A2A receptors dampen cannabinoid CB1 receptor-mediated inhibition of corticostriatal glutamatergic transmission. British Journal of Pharmacology 172:1074-1086. doi: 10.1111/bph.12970.

Lemos C, Pinheiro BS, Beleza RO, Marques JM, Rodrigues RJ, Cunha RA, Rial D, Köfalvi A (2015) Adenosine A2B receptor activation stimulates glucose uptake in the mouse forebrain. Purinergic Signalling 11:561-569. doi: 10.1007/s11302-015-9474-3.

Other information: 
 
   
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