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2025Pouladi MA and Petersen A.Special issue: Glia and non-neuronal cells in Huntington’s disease.Journal of Huntington’s Disease. 2025;14(3):212-213. doi.org/10.1177/18796397251358289Li X, Li S, Li X-J, Nguyen HP, Petersen Å and Pouladi MA.The role of oligodendroglial dysfunction in Huntington's disease.Journal of Huntington’s Disease. 2025;14(3):270-278. doi: 10.1177/18796397251358017. Bergh S, C
https://www.huntington-research.lu.se/publications - 2025-08-23
Mikrouli E, Wörtwein G, Soylu R, Mathé AA and Petersén Å.Translational Neuroendocrine Research Unit, Department of Experimental Medical Sciences, Lund University, Lund 22184, Sweden.Neuropeptides 45(6): 401-406 (2011)AbstractThe Flinders Sensitive Line (FSL) rat is a genetic animal model of depression that displays characteristics similar to those of depressed patients including lower body weight,
https://www.huntington-research.lu.se/increased-numbers-orexinhypocretin-neurons-genetic-rat-depression-model - 2025-08-23
Gil-Mohapel J, Brocardo PS, Smith R, Lagerkvist S, Li JY and Petersén Å.In H.T. Maldonado and I.M. Ortega (Eds.) Striatum: Anatomy, Functions and Role in Disease. New York, USA: Nova Publishers.AbstractBackground: Huntington’s disease (HD) is the most common polyglutamine neurodegenerative disorder. The mutation consists of an unstable expansion of CAG repeats within the coding region of the HD ge
Petersén Å.Department of Experimental Medical Science, Translational Neuroendocrine Research Unit, Lund University, Lund, Sweden.European Neurological Review 5: 49–53 (2010)AbstractHuntington’s disease (HD) is a hereditary neurodegenerative disorder that leads to premature death. There is no satisfactory treatment or cure. The disease is caused by an expanded CAG repeat in the huntingtin gene. The
Gabery S, Murphy K, Schultz K, Loy CT, McCusker E, Kirik D, Halliday G and Petersén Å.Translational Neuroendocrine Research Unit, Department of Experimental Medical Sciences, Lund University, BMC D11, 221 84, Lund, Sweden.Acta Neuropathologica 120: 777-788 (2010)AbstractHuntington disease (HD) is a fatal neurodegenerative disorder caused by expansion of a CAG repeat in the HD gene. Degeneration co
Braunstein KE, Eschbach J, Ròna-Vörös K, Soylu R, Mikrouli E, Larmet Y, Rene F, Gonzalez de Aguilar JL, Loeffler JP, Müller HP, Bucher S, Kaulisch T, Niessen HG, Tillmanns J, Fischer K, Schwalenstocker B, Kassubek J, Pichler B, Stiller D, Petersen A, Ludolph AC and Dupuis L.Department of Neurology, University of Ulm, Ulm, Germany.Human Molecular Genetics 19: 4385-4398 (2010)AbstractThe molecular m
Soneson C, Fontes M, Zhou Y, Denisov V, Paulsen JS, Kirik D and Petersén A; The Huntington Study Group PREDICT-HD investigators.Centre for Mathematical Sciences, Lund University, Sweden; Brain Repair and Imaging in Neural Systems, Department of Experimental Medical Science, BMC D11, Lund University, Sweden; Lund University Bioimaging Center, Lund University, Sweden.Neurobiology of Disease 40: 531-
Hult S, Schultz K, Soylu R and Petersén Å.Translational Neuroendocrine Research Unit, Department of Experimental Medical Sciences, Lund University, Sweden.Current Drug Targets 11: 1237-1249 (2010)AbstractHuntington's disease (HD) is a fatal hereditary neurodegenerative disorder without satisfactory treatments nor a cure. It is caused by a CAG repeat expansion in the huntingtin gene. The clinical s
https://www.huntington-research.lu.se/hypothalamic-and-neuroendocrine-changes-huntingtons-disease - 2025-08-23
Schultz K, Nilsson K, Nielsen JE, Lindquist SG, Hjermind LE, Andersen BB, Wallin A, Nilsson C and Petersén Å.European Journal of Neurology 17: 456- 460 (2010)AbstractBACKGROUND: Previous studies have indicated that transthyretin (TTR) levels in cerebrospinal fluid (CSF) are altered in depression and dementia. The present study aimed to investigate whether CSF TTR can be used to discriminate betwee
Bode FJ, Stephan M, Wiehager S, Nguyen HP, Björkqvist M, von Hörsten S, Bauer A and Petersén Å.Behavioural Brain Research 205: 175-182 (2009)AbstractHuntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the HD gene. Besides psychiatric, motor and cognitive symptoms, HD patients suffer from sleep disturbances. In order to screen a rat model transgenic for HD
Wiehager S, Beiderbeck D, Gruber S, El Khoury A, Waamsteker J, Neumann I, Mathé A* and Petersén Å*.Neurobiology of Disease 34: 375-380 (2009) *equal contributionAbstractThe neurobiological bases of mood disorders remain elusive but both monoamines and neuropeptides may play important roles. The neuropeptide cocaine and amphetamine regulated transcript (CART) was shown to induce anxiety-like behavi
Dupuis L, Petersen Å and Weydt P.Handbook of Clinical Neurology 157: 749-760 (2018)AbstractAmyotrophic lateral sclerosis (ALS) is the major adult-onset motor neuron disease, and is clinically, pathologically, and genetically associated with frontotemporal dementia, the second cause of dementia in the elderly. Here, we review the evidence linking thermoregulation and ALS. Indeed, while ALS is not c
https://www.huntington-research.lu.se/thermoregulation-amyotrophic-lateral-sclerosis - 2025-08-23
Pouladi M, Graham RK, Karasinska JM, Xie Y, Dar Santos R, Petersén Å, and Hayden MR1 Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, V6T 1Z3 Canada 2 Centre for Molecular Medicine and Therapeutics, Child and Family Research Institute, Vancouver, British Columbia, V5Z 4H4 Canada 3 Translational Neuroendocrine Research Unit, Department of Experimental Med
Schultz K, Wiehager S, Nilsson K, Nielsen JE, Lindquist SG, Hjermind LE, Andersen BB, Wallin A, Nilsson CF and Petersén Å.Neuroscience Letters 453: 104-106 (2009)AbstractDementia with Lewy bodies (DLB) is the second most common form of neurodegenerative dementia after Alzheimer's disease (AD). The underlying neurobiological mechanism of DLB is not fully understood and no generally accepted biomark
https://www.huntington-research.lu.se/reduced-csf-cart-dementia-lewy-bodies - 2025-08-23
Petersén Å, Hult S and Kirik D.Neurodegenerative Diseases 6: 154-164 (2009)AbstractHuntington's disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene. Although it is characterized by progressive motor impairments, cognitive changes and psychiatric disturbances are major components of the disease. In addition, recent studies have shown that other non-m
https://www.huntington-research.lu.se/huntingtons-disease-new-perspectives-based-neuroendocrine-changes-rodent-models - 2025-08-23
Petersén Å and Lundberg L.Läkartidningen 106: 1273-1276 (2009)Link to the article (in Swedish)
https://www.huntington-research.lu.se/neuroleptic-malignant-syndrome-rare-diagnosis-high-mortality - 2025-08-23
Brundin L, Björkqvist M, Träskman-Bendz L and Petersén Å.Journal of Affective Disorders 113: 179-182 (2009)AbstractBACKGROUND:The orexins (hypocretins) and cocaine and amphetamine regulated transcript (CART) are hypothalamic peptides involved in the regulation of sleep and appetite. We have previously shown that levels of both orexin-A and CART in the cerebrospinal fluid (CSF) are related to speci
https://www.huntington-research.lu.se/increased-orexin-levels-cerebrospinal-fluid-first-year-after-suicide-attempt - 2025-08-23
Petersén Å, Wörtwein G, Gruber SH, El-Khoury A and Mathé AA.Neuroscience Letters 451(2): 148-151 (2009)AbstractA prevailing hypothesis is that neurogenesis is reduced in depression and that the common mechanism for antidepressant treatments is to increase it in adult hippocampus. Reduced neurogenesis has been shown in healthy rats exposed to stress, but it has not yet been demonstrated in depresse
Bode F, Stephan M, Suhling H, Pabst R, Straub RH, Raber KA, Bonin M, Nguyen HP, Riess O, Bauer A, Sjoberg C, Petersén Å and von Horsten S.Human Molecular Genetics 17(17): 2595-2609 (2008)AbstractRecent clinical studies have highlighted that female sex hormones represent potential neuroprotective mediators against damage caused by acute and chronic brain diseases. This evidence has been confirmed b
Petersén Å, Wörtwein G, Gruber S and Mathé A.Neuroscience letters 436(3): 305-308 (2008)AbstractHippocampal neurogenesis is potentially implicated in etiology of depression and as the final common mechanism underlying antidepressant treatments. However, decreased neurogenesis has not been demonstrated in depressed patients and, in animals, reduced cytogenesis was shown in healthy rats exposed to s
