The NeuroCardioMetabol Group
Our research focus is on the pathophysiological mechanisms at the basis of the complications of diabetes such as stroke, endothelial dysfunction, heart failure and dementia. We also work on the identification of new therapies, with special focus on the effects mediated by incretins. Our research is translational as we use preclinical experimental models and perform clinical research with randomized clinical studies and epidemiological methods.
Thomas Nyström, Professor, joint leadership of the group
Cesare Patrone, Associate Professor, joint leadership of the group
Vladimer Darsalia, Assistant professor, responsible of the preclinical in vivo activities
David Nathanson, Senior research fellow, responsible of clinical stroke
Martin Larsson, MD and PhD student
Grazyna Lietzau, Post doc, preclinical
Hiranya Pintana, Post doc, preclinical
Ingrid Lovise Augestad, Post doc, preclinical
Fausto Chiazza, Post doc, preclinical
The group has ongoing partnerships with Professors Gilberto Fisone, Claes-Göran Östensson, Henrik Druid, Tomas Hökfelt, Helena Erlandsson Harris (KI); with Associate Professors Sergiu-Bogdan Catrina , André Fisahn, Jan Kehr, Camilla Krizhanovskii, Martin Holzman, Ulrik Sartipy, Anna-Norhammar (KI); with Professor Jan Eriksson (Uppsala University); with Professor Carina Mallard and Dr. Maria E Johansson (University of Gothenburg); with Professor Dan Lindholm (University of Helsinki); with Dr. Stefania Ceruti and Giulia Magni (University of Milan), Dr Fausto Chiazza and Professor Massimo Collino (Turin University) and with Professor Mariagrazia Grilli (Novara University). We also have an ongoing collaboration with Boehringer Ingelheim Pharma GmbH & Co. KG, Germany, since 2011.
We were the first to demonstrate (Nyström et al AJP 2004) that the incretin hormone glucagon-like peptide 1 (GLP-1) improves endothelial function in type 2 diabetic (T2D) patients. We were also the first group to show the anti-stroke efficacy of incretin mimetics and of dipeptidyl peptidase-4 inhibitors in animal models of T2D (Darsalia et al, Cli Sci 2012; Darsalia et al 2013 Diabetes).
We also showed that T1D patients have a dire prognosis after coronary artery bypass grafting (CABG) than non-diabetics (Holzmann et al JACC 2015) and that glycemic control is a key predictor for mortality in T1D after CABG (Nyström et al JACC 2015) as for T2D (Kuhl et al Int J Cardiol 2015). Moreover we are participating in population based studies evaluating prevalence, incidence and life expectancy of pharmacologically treated T2D patients (Norhammar et al, Diabetologia 2016) and effects of novel oral glucose lowering drugs (Nyström et al, Diabetes obesity and metabolism, 2017).
Preclinically, we recently showed that the anti-stroke efficacy by DPP-4 inhibitors is not mediated via GLP-1 (Darsalia et al Diabetes Obes Metab 2016) but SDF1a (Chiazza et al. Cardiovasc Diabetol 2017). We also provided new insights on how T2D impairs neuroplasticity and neurogenesis during aging (Lietzau et al Psychoneuroendocrinol. 2017 and Acta Neuropathol Commun 2018, Mansouri et al PLOS One 2016, Hussain S et al J Alzheimers Dis. 2014); observations that could be at the basis of decreased olfaction and cognitive decline in T2D.
Our Research group has been recently financed by:
- Svensk Förening för Diabetologi; 2019 (Lietzau))
- The Swedish Research Council (Vetenskaprådet); 2018-2021 (Patrone)
- The Swedish Heart-Lung Foundation; 2016-2019 (Nyström)
- European Foundation for the Study of Diabetes (EFSD)/Sanofi European Diabetes Research Programme in Macrovascular Complications; 2019 (Patrone)
- Diabetesfonden; 2017 (Nyström)
- Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse; 2012-2017 (Patrone)
- NovoNordisk foundation; 2018 (Nyström)
- EFSD Albert Renold Travel Fellowship Programme to Dr Fausto Chiazza; 2018
- Karolinska Institutet (Foundation for Geriatric Diseases); 2019 (Pintana).
- KI Stiftelser och Fonder; 2019 (Lietzau)
- Åhlén Stiftelse; 2012-2018 (Patrone)
- Stiftelsen för Gamla Tjänarinnor; 2019 (Lietzau)
- O. E. och Edla Johanssons Stiftelse; 2016-2018 (Patrone)
- Magnus Bergvalls Stiftelse; 2016 (Patrone)
- STROKE Riksförbundet; 2018-2020 (Patrone)
- Stiftelsen för Gamla Tjänarinnor; 2017 (Darsalia)
- Syskonen Svensson Stiftelse; 2017 (Patrone)
- ALF; 2016-2020 (Nyström)
- EFSD; 2011 (Darsalia)
- EFSD; 2009 and 2013 (Patrone)
- Diabetes Wellness; 2010 (Patrone)
The effect of DPP-4 inhibition to improve functional outcome after stroke is mediated by the SDF-1α/CXCR4 pathway.
Cardiovasc Diabetol 2018 05;17(1):60
PCI Versus CABG in Patients With Type 1 Diabetes and Multivessel Disease.
J. Am. Coll. Cardiol. 2017 Sep;70(12):1441-1451
Glycemic Control in Type 1 Diabetes and Long-Term Risk of Cardiovascular Events or Death After Coronary Artery Bypass Grafting.
J. Am. Coll. Cardiol. 2015 Aug;66(5):535-43
Effects of glucagon-like peptide-1 on endothelial function in type 2 diabetes patients with stable coronary artery disease.
Am. J. Physiol. Endocrinol. Metab. 2004 Dec;287(6):E1209-15
Type 2 diabetes impairs odour detection, olfactory memory and olfactory neuroplasticity; effects partly reversed by the DPP-4 inhibitor Linagliptin.
Acta Neuropathol Commun 2018 02;6(1):14
Gliptin-mediated neuroprotection against stroke requires chronic pretreatment and is independent of glucagon-like peptide-1 receptor.
Diabetes Obes Metab 2016 May;18(5):537-41
Diabetes drugs and neurological disorders: new views and therapeutic possibilities.
Lancet Diabetes Endocrinol 2014 Mar;2(3):256-62
GalR3 activation promotes adult neural stem cell survival in response to a diabetic milieu.
J. Neurochem. 2013 Oct;127(2):209-20
The DPP-4 inhibitor linagliptin counteracts stroke in the normal and diabetic mouse brain: a comparison with glimepiride.
Diabetes 2013 Apr;62(4):1289-96
Glucagon-like peptide-1 receptor activation reduces ischaemic brain damage following stroke in Type 2 diabetic rats.
Clin. Sci. 2012 May;122(10):473-83