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Progranulin bridges energy homeostasis and fronto-temporal dementia

Dupuis L1, 2, 3, Petersen A4, Weydt P31 Inserm U692, Laboratoire de Signalisations Moléculaires et Neurodégénérescence, 67085Strasbourg, France2 Université de Strasbourg, Faculté de Médecine, UMRS692, 67085Strasbourg, France3 Department of Neurology, Ulm University, 89081 Ulm, Germany4 Translational Neuroendocrine Research Unit, Department of Experimental Medical Sciences, Lund University, 22184Lu

https://www.huntington-research.lu.se/progranulin-bridges-energy-homeostasis-and-fronto-temporal-dementia - 2026-01-01

Mutant huntingtin causes metabolic imbalance by disruption of hypothalamic neurocircuits

Hult S*, Soylu R*, Björklund T, Belgardt B F, Mauer J, Brüning J C, Kirik D and Petersén Å.Translational Neuroendocrine Research Unit, Department of Experimental Medical Sciences, Lund University, Lund 22184, Sweden.Cell Metabolism 13: 428-439 (2011) *equal contributionAbstractIn Huntington's disease (HD), the mutant huntingtin protein is ubiquitously expressed. The disease was considered to be li

https://www.huntington-research.lu.se/mutant-huntingtin-causes-metabolic-imbalance-disruption-hypothalamic-neurocircuits - 2026-01-01

Eating and hypothalamus changes in behavioral-variant frontotemporal dementia

Piguet O, Petersén A, Yin Ka Lam B, Gabery S, Murphy K, Hodges JR and Halliday GM.Neuroscience Research Australia, Sydney, Australia.Annals of Neurology 69: 312-319 (2011)AbstractOBJECTIVE: Behavioral-variant frontotemporal dementia (bvFTD) is a progressive neurodegenerative brain disorder, clinically characterized by changes in cognition, personality, and behavior. Marked disturbances in eating b

https://www.huntington-research.lu.se/eating-and-hypothalamus-changes-behavioral-variant-frontotemporal-dementia - 2026-01-01

Publications

2025Aziz NA, Claassen D, Petersén Å and Weydt P.β-Blocker effects in huntington's disease: A caution on clinical interpretation.European Huntington's Disease Network and the Huntington Study Group. Published online December 15, 2025. doi:10.1177/18796397251401745.Oraha J, Wagner R, Bergh S, Lee NJ, Kirik D and Petersén Å.Differential effects of overexpression of mutant huntingtin and TDP-43 in ago

https://www.huntington-research.lu.se/publications - 2026-01-01

Increased numbers of orexin/hypocretin neurons in a genetic rat depression model

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 - 2026-01-01

Impaired Nigrostriatal Dopaminergic Neurotransmission in Huntington’s Disease: Insights from the R6/1 Transgenic Mouse Model

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

https://www.huntington-research.lu.se/impaired-nigrostriatal-dopaminergic-neurotransmission-huntingtons-disease-insights-r61-transgenic - 2026-01-01

The Role of Hypothalamic and Neuroendocrine Changes in the Pathogenesis of Huntington’s Disease – Current Understanding and Implications for Future Treatments

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

https://www.huntington-research.lu.se/role-hypothalamic-and-neuroendocrine-changes-pathogenesis-huntingtons-disease-current-understanding - 2026-01-01

Changes in key hypothalamic neuropeptide populations in Huntington disease revealed by neuropathological analyses

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

https://www.huntington-research.lu.se/changes-key-hypothalamic-neuropeptide-populations-huntington-disease-revealed-neuropathological - 2026-01-01

A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons

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

https://www.huntington-research.lu.se/point-mutation-dynein-heavy-chain-gene-leads-striatal-atrophy-and-compromises-neurite-outgrowth - 2026-01-01

Early changes in the hypothalamic region in prodromal Huntington disease revealed by MRI analysis

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-

https://www.huntington-research.lu.se/early-changes-hypothalamic-region-prodromal-huntington-disease-revealed-mri-analysis - 2026-01-01

Hypothalamic and Neuroendocrine Changes in Huntington's Disease

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 - 2026-01-01

Transthyretin as a potential CSF biomarker for Alzheimer's disease and dementia with Lewy bodies: effects of treatment with cholinesterase inhibitors.

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

https://www.huntington-research.lu.se/transthyretin-potential-csf-biomarker-alzheimers-disease-and-dementia-lewy-bodies-effects-treatment - 2026-01-01

Increased numbers of motor activity peaks during light cycle are associated with reductions in adrenergic alpha(2)-receptor levels in a transgenic Huntington disease rat model

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

https://www.huntington-research.lu.se/increased-numbers-motor-activity-peaks-during-light-cycle-are-associated-reductions-adrenergic - 2026-01-01

Increased levels of cocaine and amphetamine regulated transcript (CART) in two animal models of depression and anxiety

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

https://www.huntington-research.lu.se/increased-levels-cocaine-and-amphetamine-regulated-transcript-cart-two-animal-models-depression-and - 2026-01-01

Thermoregulation in amyotrophic lateral sclerosis

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 - 2026-01-01

Prevention of depressive behaviour in the YAC128 mouse model of Huntington disease by mutation at residue 586 of huntingtin

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

https://www.huntington-research.lu.se/prevention-depressive-behaviour-yac128-mouse-model-huntington-disease-mutation-residue-586 - 2026-01-01

Reduced CSF CART in dementia with Lewy bodies

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 - 2026-01-01

Huntington’s disease - new perspectives based on neuroendocrine changes in rodent models

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 - 2026-01-01

Increased orexin levels in the cerebrospinal fluid the first year after a suicide attempt

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 - 2026-01-01