Brundin L, Björkqvist M, Petersén Å and Träskman-Bendz L.European Neuropsychopharmacology 17: 573-579 (2007)AbstractOrexins are neuropeptides selectively expressed in a small number of neurons in the lateral-posterior hypothalamus. We measured orexin-A in the cerebrospinal fluid (CSF) of 66 patients with major depressive disorder (MDD), dysthymia and adjustment disorder after a suicide attempt. Bl

https://www.huntington-research.lu.se/reduced-orexin-levels-cerebrospinal-fluid-suicidal-patients-major-depressive-disorder - 2025-07-25

Van Raamsdonk JM, Murphy Z, Selva DM, Hamidizadeh R, Pearson J, Petersen Å, Björkqvist M, Muir C, Mackenzie IR, Hammond GL, Vogl AW, Hayden MR and Leavitt BR.Neurobiology of Disease 26: 512-520 (2007)AbstractHuntington disease (HD) is an adult onset, neurodegenerative disorder that results from CAG expansion in the HD gene. Recent work has demonstrated testicular degeneration in mouse models of HD

https://www.huntington-research.lu.se/testicular-degeneration-huntington-disease - 2025-07-25

Petersén Å and Björkqvist M.European Journal of Neuroscience 24: 961-967 (2006)AbstractHuntington's disease (HD) is a hereditary and fatal disorder caused by an expanded CAG triplet repeat in the HD gene, resulting in a mutant form of the protein huntingtin. Wild-type and mutant huntingtin are expressed in most tissues of the body but the normal function of huntingtin is not fully known. In HD, th

https://www.huntington-research.lu.se/hypothalamic-endocrine-aspects-huntingtons-disease - 2025-07-25

Baldo B, Sajjad MU, Cheong RY, Bigarreau J, Vijayvargia R, McLean C, Perrier AL, Seong IS, Halliday G, Petersén Å and Kirik D.ENeuro 5 (4). pii: ENEURO.0234-18.2018 (2018)AbstractThe neurodegenerative Huntington's disease (HD) is caused by a polyglutamine (polyQ) amplification in the huntingtin protein (HTT). Currently there is no effective therapy available for HD; however, several efforts are di

https://www.huntington-research.lu.se/quantification-total-and-mutant-huntingtin-protein-levels-biospecimens-using-novel-alphalisa-assay - 2025-07-25

Björkqvist M*, Petersén Å*, Nielsen J, Ecker D, Mulder H, Hayden M, Landwehrmeyer B, Brundin P and Leavitt B.Clinical Genetics 70: 78-79 (2006) *equal contribution Full text article    

https://www.huntington-research.lu.se/cerebrospinal-fluid-levels-orexin-levels-are-not-useful-biomarker-huntington-disease - 2025-07-25

Björkqvist M, Petersén Å, Bacos K, Isaacs J, Norlén P, Gil J, Popovic N, Sundler F, Bates GP, Tabrizi SJ, Brundin P and Mulder H.Human Molecular Genetics 15: 1713-1721 (2006)AbstractHuntington's disease (HD) is characterized by a triad of motor, psychiatric and cognitive symptoms. Although many of these symptoms are likely to be related to central nervous system pathology, others may be due to cha

https://www.huntington-research.lu.se/progressive-alterations-hypothalamic-pituitary-adrenal-axis-r62-transgenic-mouse-model-huntingtons - 2025-07-25

Winkler C, Gil JMAC, Araújo IM, Rieß O, Skripuletz I, von Hörsten S and Petersén Å.Brain Research Bulletin 69: 306-310 (2006)AbstractHuntington's disease (HD) is a hereditary neurodegenerative disorder caused by a CAG repeat expansion in the HD gene. Excitotoxic cell damage by excessive stimulation of glutamate receptors has been hypothesized to contribute to the pathogenesis of HD. Transgenic mou

https://www.huntington-research.lu.se/normal-sensitivity-excitotoxicity-transgenic-huntingtons-disease-rat - 2025-07-25

Gawlik KI, Li J-Y, Petersén Å and M Durbeej.Human Molecular Genetics 15: 2690-2700 (2006)AbstractAbsence of laminin alpha2 chain leads to a severe form of congenital muscular dystrophy (MDC1A) associated with peripheral neuropathy. Hence, future therapies should be aimed at alleviating both muscle and neurological dysfunctions. Pre-clinical studies in animal models have mainly focused on ameliorat

https://www.huntington-research.lu.se/laminin-alpha1-chain-improves-laminin-alpha2-chain-deficient-peripheral-neuropathy - 2025-07-25

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.Human Molecular Genetics 14: 39-47 (2005).AbstractHuntington's disease (HD) is a devastating neurodegenerative disorder caused by an expanded CAG repeat in the gene encoding huntingtin, a protein of unknown function. Mutant huntingtin f

https://www.huntington-research.lu.se/orexin-loss-huntingtons-disease - 2025-07-25

Puschban Z, Stefanova N, Petersén Å, Winkler C, Brundin P, Poewe IW and Wenning GP.Brain Research Bulletin 68: 54-58 (2005)AbstractEmbryonic transplantation has been considered as an alternative treatment strategy for drug resistant parkinsonian symptoms in multiple system atrophy. So far our group has created a number of animal models of striatonigral degeneration, the core pathology underlying p

https://www.huntington-research.lu.se/evidence-dopaminergic-re-innervation-embryonic-allografts-optimized-rat-model-parkinsonian-variant - 2025-07-25

Gil JM, Mohapel P, Araujo IM, Popovic N, Li JY, Brundin P and Petersen Å.Neurobiology of Disease 3: 744-751 (2005)AbstractWe investigated whether cell proliferation and neurogenesis are altered in R6/2 transgenic Huntington's disease mice. Using bromodeoxyuridine (BrdU), we found a progressive decrease in the number of proliferating cells in the dentate gyrus of R6/2 mice. This reduction was detec

https://www.huntington-research.lu.se/reduced-hippocampal-neurogenesis-r62-transgenic-huntingtons-disease-mice - 2025-07-25

Petersén Å, Stewénius Y, Björkqvist M and Gisselsson D.BMC Cell Biology 6: 34 (2005)AbstractBACKGROUND: Huntington's disease (HD) is a hereditary neurodegenerative disorder caused by a CAG repeat expansion in the HD gene. The huntingtin protein expressed from HD has an unknown function but is suggested to interact with proteins involved in the cell division machinery. The R6/2 transgenic mouse is

https://www.huntington-research.lu.se/euploidy-somatic-cells-r62-transgenic-huntingtons-disease-mice - 2025-07-25

Smith R, Petersén Å, Bates GP, Brundin P and Li JY.Neurobiology of Disease 20: 673-84 (2005)AbstractHuntington's disease (HD) is a hereditary neurodegenerative disorder characterized by progressive psychiatric, cognitive, and motor disturbances. We studied the expression of synaptic vesicle proteins in the R6/1 transgenic mouse model of HD. We observed that the levels of rabphilin 3A, a protein in

https://www.huntington-research.lu.se/depletion-rabphilin-3a-transgenic-mouse-model-r61-huntingtons-disease-possible-culprit-synaptic - 2025-07-25

Björkqvist M, Fex M, Renstrom E, Wierup N, Petersén Å, Gil J, Bacos K, Popovic N, Li JY, Sundler F, Brundin P and Mulder H.Human Molecular Genetics 14: 565-574 (2005)AbstractDiabetes frequently develops in Huntington's disease (HD) patients and in transgenic mouse models of HD such as the R6/2 mouse. The underlying mechanisms have not been clarified. Elucidating the pathogenesis of diabetes in HD

https://www.huntington-research.lu.se/r62-transgenic-mouse-model-huntingtons-disease-develops-diabetes-due-deficient-beta-cell-mass-and - 2025-07-25

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 - 2025-07-25

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 - 2025-07-25

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 - 2025-07-25

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 - 2025-07-25

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 - 2025-07-25

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 - 2025-07-25