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mHTT Seeding Activity: A Marker of Disease Progression and Neurotoxicity in Models of Huntington's Disease

Ast A, Buntru A, Schindler F, Hasenkopf R, Schulz A, Brusendorf L, Klockmeier K, Grelle G, McMahon B, Niederlechner H, Jansen I, Diez L, Edel J, Boeddrich A, Franklin SA, Baldo B, Schnoegl S, Kunz S, Purfürst B, Gaertner A, Kampinga HH, Morton AJ, Petersén Å, Kirstein J, Bates GP and Wanker EE.Molecular Cell 71 (5): 675-688.(2018)AbstractSelf-propagating, amyloidogenic mutant huntingtin (mHTT) agg

https://www.huntington-research.lu.se/mhtt-seeding-activity-marker-disease-progression-and-neurotoxicity-models-huntingtons-disease - 2025-11-29

Combining neuroprotective treatment of embryonic nigral donor tissue with mild hypothermia of the graft recipient

Karlsson J, Petersén Å, Gidö G, Wieloch T and Brundin P.Cell Transplantation 14: 301-309 (2005)AbstractAround 80-95% of the immature dopaminergic neurons die when embryonic ventral mesencephalic tissue is transplanted. Cell death occurs both during the preparation of donor tissue and after graft implantation, but the effect of combining successful neuroprotective treatments before and after transp

https://www.huntington-research.lu.se/combining-neuroprotective-treatment-embryonic-nigral-donor-tissue-mild-hypothermia-graft-recipient - 2025-11-29

Proteolysis of NR2B by calpain in the hippocampus of epileptic rats

Araujo IM, Xapelli S, Gil JM, Mohapel P, Petersén Å, Pinheiro PS, Malva JO, Bahr BA, Brundin P and Carvalho CM.Neuroreport 16: 393-396 (2005)AbstractOveractivation of N-methyl-D-aspartate receptors is known to mediate excitotoxicity due to excessive entry of calcium, leading to the activation of several calcium-dependent enzymes. Calpains are calcium-activated proteases that appear to play a role

https://www.huntington-research.lu.se/proteolysis-nr2b-calpain-hippocampus-epileptic-rats - 2025-11-29

Reduction of GnRH and infertility in the R6/2 mouse model of Huntington’s disease

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 - 2025-11-29

Asialoerythropoetin is not effective in the R6/2 line of Huntington's disease mice

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 - 2025-11-29

Evidence for dysfunction of the nigrostriatal pathway in the R6/1 line of transgenic Huntington's disease mice

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 - 2025-11-29

Maintenance of susceptibility to neurodegeneration following intrastriatal injections of quinolinic acid in a new transgenic mouse model of Huntington's disease

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 - 2025-11-29

Huntington's Disease: the mystery unfolds?

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 - 2025-11-29

Mice transgenic for exon 1 of the Huntington's disease gene display reduced striatal sensitivity to neurotoxicity induced by dopamine and 6-hydroxydopamine

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 - 2025-11-29

Expanded CAG repeats in exon 1 of the Huntington's Disease gene stimulate dopamine-mediated striatal neuron autophagy and degeneration

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 - 2025-11-29

Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death

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 - 2025-11-29

Visit us

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 - 2025-11-29

Former team members

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 - 2025-11-29

PhD thesis books

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 - 2025-11-29

Psychiatric and metabolic disturbances in experimental models of Huntington's disease

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 - 2025-11-29

New perspectives on pathology in Huntington's disease - characterization of hypothalamic changes

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 - 2025-11-29

Hypothalamic and Metabolic Dysfunction in Genetic Models of Huntington's Disease

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 - 2025-11-29

Microstructural white matter alterations and hippocampal volumes are associated with cognitive deficits in craniopharyngioma

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 - 2025-11-29

Åsa Petersén, MD PhD

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 - 2025-11-29

Curriculum Vitae - Åsa Petersén

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 - 2025-11-29