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Papalexi E, Persson A, Björkqvist M, Petersén Å, Woodman B, Bates GP, Sundler F, Mulder H, Brundin P and Popovic N.European Journal of Neuroscience 22: 1541-1546 (2005)AbstractReductions in testosterone and luteinizing hormone levels and reduced sexual functions have been reported in Huntington's disease (HD) patients. Atrophy of the reproductive organs and loss of fertility have also been observe

https://www.huntington-research.lu.se/reduction-gnrh-and-infertility-r62-mouse-model-huntingtons-disease - 2026-05-09

Gil MAC J, Leist M, Popovic N, Brundin P and Petersén Å.BMC Neuroscience 5: 17 (2004)AbstractBACKGROUND:Huntington's disease (HD) is a hereditary neurodegenerative disorder caused by an expanded CAG repeat in the HD gene. Both excitotoxicity and oxidative stress have been proposed to play important roles in the pathogenesis of HD. Since no effective treatment is available, this study was designed

https://www.huntington-research.lu.se/asialoerythropoetin-not-effective-r62-line-huntingtons-disease-mice - 2026-05-09

Petersén Å, Puschban Z, Lotharius J, NicNiocaill B, Wiekop B, O´Connor, WT and Brundin P.Neurobiology of Disease 11: 134-146 (2002)AbstractThe present multidisciplinary study examined nigrostriatal dopamine and striatal amino acid transmission in the R6/1 line of transgenic Huntington's disease (HD) mice expressing exon 1 of the HD gene with 115 CAG repeats. Although the number of tyrosine hydroxy

https://www.huntington-research.lu.se/evidence-dysfunction-nigrostriatal-pathway-r61-line-transgenic-huntingtons-disease-mice - 2026-05-09

Petersén Å, Chase K, Puschban Z, DiFiglia M, Brundin P and Aronin N.Experimental Neurology 175: 297-300 (2002)AbstractA transgenic mouse model of Huntington's disease (R6/1 and R6/2 lines) expressing exon 1 of the HD gene with 115-150 CAG repeats resisted striatal damage following injection of quinolinic acid and other neurotoxins. We examined whether excitotoxin resistance characterizes mice with

https://www.huntington-research.lu.se/maintenance-susceptibility-neurodegeneration-following-intrastriatal-injections-quinolinic-acid-new - 2026-05-09

Petersén Å and Brundin P.International Review of Neurobiology 53: 315-339 (2002) SummaryThe Huntington's disease (HD) has stimulated novel clinical drug trials based on the ideas about mechanisms of cell death in the disorder. A recent study investigated the effects of remacemide and coenzyme Q on progression of symptoms in HD. These drugs are an N-methyl-d-aspartate (NMDA) antagonist and a mitoch

https://www.huntington-research.lu.se/huntingtons-disease-mystery-unfolds - 2026-05-09

Petersén Å, Hansson O, Puschban Z, Sapp E, Romero N, Castilho RF, Sulzer D, Rice M, DiFiglia M, Przedborski S and Brundin P.European Journal of Neuroscience 14: 1-13 (2001)AbstractHuntington's disease is an autosomal dominant hereditary neurodegenerative disorder characterized by severe striatal cell loss. Dopamine (DA) has been suggested to play a role in the pathogenesis of the disease. We have

https://www.huntington-research.lu.se/mice-transgenic-exon-1-huntingtons-disease-gene-display-reduced-striatal-sensitivity-neurotoxicity - 2026-05-09

Petersén Å, Larsen KE, Behr GG, Romero N, Przedborski S, Brundin P and Sulzer D.Human Molecular Genetics 10: 1243-1254 (2001)AbstractHuntington's disease (HD) is caused by an expanded CAG repeat in exon 1 of the gene coding for the huntingtin protein. The cellular pathway by which this mutation induces HD remains unknown, although alterations in protein degradation are involved. To study intrinsic

https://www.huntington-research.lu.se/expanded-cag-repeats-exon-1-huntingtons-disease-gene-stimulate-dopamine-mediated-striatal-neuron - 2026-05-09

Petersén Å, Larsen KE, Behr GG, Romero N, Przedborski S, Brundin P, and Sulzer D.Section for Neuronal Survival, Wallenberg Neuroscience Center, Lund University, Lund, SwedenBrain Research Bulletin 56(3-4): 331-335 (2001)AbstractIn hereditary Huntington's disease, a triplet repeat disease, there is extensive loss of striatal neurons. It has been shown that brain-derived neurotrophic factor (BDNF) p

https://www.huntington-research.lu.se/brain-derived-neurotrophic-factor-inhibits-apoptosis-and-dopamine-induced-free-radical-production - 2026-05-09

The Translational Neuroendocrine Research Unit (TNU) is located in the Biomedical Center (BMC) in Lund in the south of Sweden.Our visiting address is Klinikgatan 32, building D, floor 11.How to get to LundFrom Copenhagen Airport (CPH)Copenhagen airport Kastrup is Denmark's international airport, and is much closer to Lund than the airports in Stockholm. Here you have direct flights from most Europ

https://www.huntington-research.lu.se/visit-us - 2026-05-09

Rachel Cheong Former Postdoctoral fellow, 2013-2014, and Assistant Researcher, 2015-2021. Publications from TNU: 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: 1

https://www.huntington-research.lu.se/former-team-members - 2026-05-09

During the years 2014-2016 TNU has had three PhD students defending their theses. Sofia Hult Lundh: Psychiatric and metabolic disturbances in experimental models of Huntington’s disease Sanaz Gabery: New perspectives on pathology in Huntington's disease - characterization of hypothalamic changes Rana Soylu Kurcharz: Hypothalamic and Metabolic Dysfunction in Genetic Models of Huntington's Disease P

https://www.huntington-research.lu.se/phd-thesis-books - 2026-05-09

English summary Non-motor symptoms and signs such as metabolic and psychiatric disturbances have been reported to occur early in Huntington's disease (HD), a fatal neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene.However, there is a lack of understanding of the underlying neurobiological mechanisms responsible for the early non-motor features.The hypothalamus has

https://www.huntington-research.lu.se/psychiatric-and-metabolic-disturbances-experimental-models-huntingtons-disease - 2026-05-09

English summary Huntington’s disease (HD) is a neurodegenerative disorder caused by an expansion of the CAG repeat in the huntingtin gene. Non-motor symptoms and signs such as psychiatric disturbances and metabolic dysfunction are also part of the disease manifestation. These symptoms often precede the motor symptoms by decades. The hypothalamus is an area in the brain involved in the regulation o

https://www.huntington-research.lu.se/new-perspectives-pathology-huntingtons-disease-characterization-hypothalamic-changes - 2026-05-09

English summary Huntington’s disease (HD) is caused by a CAG trinucleotide repeat expansion in the huntingtin (HTT) gene. HD is an inherited progressive neurodegenerative disorder manifested by the wide array of motor dysfunctions, as well as non-motor symptoms. The latter include metabolic dysfunction and psychiatric deficits, such as depression and anxiety, are often observed in patients and ani

https://www.huntington-research.lu.se/hypothalamic-and-metabolic-dysfunction-genetic-models-huntingtons-disease - 2026-05-09

Fjalldal S, Follin C, Svärd D, Rylander L, Gabery S, Petersen Å, Van Westen D, Sundgren P, Bjorkman-Burtscher I, Lätt J, Ekman B, Johanson A and Erfurth EM.European Journal of Endocrinology 178 (6): 577-587 (2018)AbstractCONTEXT:Patients with craniopharyngioma (CP) and hypothalamic lesions (HL) have cognitive deficits. Which neural pathways are affected is unknown.OBJECTIVE:To determine whether th

https://www.huntington-research.lu.se/microstructural-white-matter-alterations-and-hippocampal-volumes-are-associated-cognitive-deficits-0 - 2026-05-09

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 rece

https://www.huntington-research.lu.se/team/asa-petersen-md-phd - 2026-05-09

Full Name : Åsa Petersén Date of Birth: October 25th, 1974 Nationality: Swedish Address: Translational Neuroendocrinology (TNU), BMC D11, 221 84 Lund Phone: +46 46 222 16 86 E-mail address: Asa.Petersen@med.lu.se Professional appointments 2017-present Professor in Medical Research with specialization in Neuroscience, Medical Faculty, LU, combined position (s k förenad anställning) as Senior Consul

https://www.huntington-research.lu.se/curriculum-vitae-asa-petersen - 2026-05-09

Professor Åsa Petersén received the Fernström award 2018 for younger, successful researchers (Eric K Fernströms Svenska Pris 2018). The prize is awarded six researches at different Medical Faculties in Sweden, where each and one receives the sum of SEK 100 000. The Lund award ceremony took place on November 7 at “Forskningens dag”.  Best Neurobiology section PhD thesis 2016 was awarded Dr. Rana So

https://www.huntington-research.lu.se/awards - 2026-05-09

Sanaz Gabery defended her doctoral thesis in TNU in 2015, was employed at Novo Nordisk A/S in Denmark and returned to Lund University in 2018. From 2017 to 2022 she combined her research with medical studies at Lund University. One of her projects aimed to determine the role of white matter pathology for the development and treatment of Huntington’s disease. Recent studies performed by Gabery and

https://www.huntington-research.lu.se/team/sanaz-gabery-phd - 2026-05-09

Translational studies addressing the main aims of the research group use experimental models and clinical material from patients with HD and FTD/ALS. Techniques used in the laboratory include detailed testing of motor, cognitive, social/emotional behaviours, metabolic function, stereotactic surgery, gene targeting and disease modelling using adeno-associated viral vectors (AAV), immunohistochemist

https://www.huntington-research.lu.se/translational-research-laboratory - 2026-05-09