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Åsa Petersén, MD PhD

Photo of Åsa Petersén, taken by Kennet Ruona.
Photo: Kennet Ruona

Petersén began medical school at Lund University (LU) in 1994 and started her PhD training in 1997. She received her PhD in experimental neuroscience in 2001 at the Faculty of Medicine at LU with Prof. Patrik Brundin as supervisor with a PhD thesis on Huntington’s disease (HD). She became an MD 2004 and a Reader (docent) in Neuroscience in 2006.

Petersén started her research group TNU when she received a junior researcher position (Forskarassistentjänst) at LU in 2007, funded by the Swedish Research Council (VR). Petersén then received a senior researcher position (Forskaretjänst) at Lund University funded by VR in 2009 and became a Senior Lecturer in Medical Research at Lund University in 2012. She was promoted to Full Professor in Neurocience in 2016.

Petersén has previously combined her research positions with a clinical residency in psychiatry and became specialist in psychiatry 2017. She now holds a combined position as Professor in Neuroscience and Senior Consultant in Psychiatry at LU and Region Skåne. Her clinical position is at the HD clinic in Lund. She received the prestigious Fernström Foundation award at the Faculty of Medicine at LU in 2018. She was recently appointed Wallenberg Clinical Scholar 2020-2025 with a grant support of 15,000,000 SEK from the Knut and Alice Wallenberg Foundation. 

Petersén’s research is focused on neurobiological aspects of psychiatric disorders. Her main expertise is HD. Although HD has traditionally been considered a movement disorder, it is now clear that the early psychiatric symptoms precede the motor component of the disease and that the psychiatric symptoms are the most debilitating part for the affected individuals.

Petersén has published key studies identifying early psychiatric features in several HD animal models clearly indicating neurobiological mechanisms underlying these features. Petersén’s hypothesis is that hypothalamic dysfunction is involved in causing the early psychiatric and metabolic features of HD. She has performed pioneering studies demonstrating effects on the specific emotion-regulating neuropeptides orexin and oxytocin in the hypothalamus of HD patients. Petersén’s aim is to increase the understanding of the neurobiological aspects of psychiatric symptoms in HD but also for other brain disorders including mental illness. Indeed, Petersén’s investigations of hypothalamic pathology has already extended to include other diseases such as depressive and anxiety disorder, frontotemporal dementia and ALS.   

Phone: +46 46 222 16 86
E-mail: Asa [dot] Petersen [at] med [dot] lu [dot] se (subject: Email%20from%20TNU%20webpage) (Asa[dot]Petersen[at]med[dot]lu[dot]se)

Visiting address
Translational Neuroendocrinology (TNU)
BMC House D Floor 11, Entrance from Klinikgatan 32 
(see further details on our webpage under Visit us

Postal address
Translational Neuroendocrinology (TNU), BMC D11
Department of Experimental Medical Science
Lund University
221 84 Lund, Sweden 

Key publications

Gabery S, Kwa JE, Cheong RY, Baldo B, Ferrari Bardile C, Tan B, McLean C, Georgiou-Karistianis N, Poudel GR, Halliday G, Pouladi MA and Petersén Å.
Early white matter pathology in the fornix of the limbic system in Huntington disease.
Acta Neuropathologica. 142(5): 791-806 (2021) doi: 10.1007/s00401-021-02362-8.

Gabery S,  Ahmed RA, Caga J,  Kiernan MC, Halliday GM and Petersén Å. 
Loss of the metabolism and sleep regulating neuronal populations expressing orexin and oxytocin in the hypothalamus in amyotrophic lateral sclerosis.
Neuropathology and Applied Neurobiology. First published March 23, 2021.

Baldo B, Gabery S, Soylu-Kucharz R, Cheong RY, Henningsen JB, Englund E, McLean C, Kirik D, Halliday G and Petersén Å.
SIRT1 is increased in affected brain regions and hypothalamic metabolic pathways are altered in Huntington disease.
Neuropathology and Applied Neurobiology 45 (4): 361-379 (2019)

Hult S*, Soylu R*, Björklund T, Belgardt BF, Mauer J, Brüning JC, Kirik D and Petersén Å.
Mutant huntingtin causes metabolic imbalance by disruption of hypothalamic neurocircuits.
Cell Metabolism 13: 428-439 (2011) *equal contribution

Gabery S, Murphy K, Schultz K, Loy CT, McCusker E, Kirik D, Halliday G and Petersén Å.
Changes in key hypothalamic neuropeptide populations in Huntington disease revealed by neuropathological analyses.  
Acta Neuropathologica 120: 777-788 (2010)

Petersén Å, Gil J, Maat-Schieman MLC, Björkqvist M, Tanila H, Araujo IM, Smith R, Popovic N, Wierup N, Norlén P, Li JY, Roos RAC, Sundler F, Mulder H and Brundin P.
Orexin loss in Huntington’s disease.  
Human Molecular Genetics 14: 39-47 (2005). [Commentary by: Khamsi R, Nature 432:288 (2005) and by Hurtley S, Science 307:483 (2005)]