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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

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 - 2025-08-23

Prefektbrev juni 2025.Prefektbrev maj 2025.Prefektbrev april 2025Prefektbrev mars 2025Prefektbrev februari 2025

https://www.fysik.lu.se/om-oss/prefektbrev/prefektbrev-2025 - 2025-08-23

Ormens år – utmaningar, möjligheter och vägen framåtFör drygt en vecka sedan trädde vi in i Ormens år – en tid som enligt mytologin kan föra med sig osäkerhet och kaos. Kanske började Ormens år redan tidigare, med tanke på allt som har hänt både hos oss och i världen. Vi har sett både positiva och negativa händelser, och en del utvecklingar är fortfarande oklara. Samtidigt sägs det vara ett år av

https://www.fysik.lu.se/om-oss/prefektbrev/prefektbrev-2025/prefektbrev-februari-2025 - 2025-08-23

RelevansEn av styrkorna med den fysiska institutionen är att vi har en härlig blandning av renodlad grundforskning och tillämpad forskning, samt allt däremellan – ibland på uppdrag, men annars initierat av forskarna. Vi bör därför ha ett brett spektrum av möjliga ämnen som kan passa in i studenternas och samhällets förväntningar och önskemål, och vi har alla möjligheter att attrahera de bästa stud

https://www.fysik.lu.se/om-oss/prefektbrev/prefektbrev-2025/prefektbrev-mars-2025 - 2025-08-23

Arbetsmiljöfrågor delas ofta in i den fysiska arbetsmiljön, inklusive säkerhet, och den psykosociala arbetsmiljön. Den fysiska arbetsmiljön är lättare att sätta upp regler för och följa upp. Man måste utbildas för att hantera kemikalier i ett laboratorium, vi har regelbundna skyddsronder och om något händer (som på nanolabbet nyligen) finns det rutiner och procedurer som ser till att begränsa even

https://www.fysik.lu.se/om-oss/prefektbrev/prefektbrev-2025/prefektbrev-april-2025 - 2025-08-23

Om statlig styrningDet har diskuterats i forskningspropositionen, i forskarsamhället och i media, frågan om vilken som är den bästa styrformen för Sveriges universitet. Lunds universitet är en statlig myndighet, på gott och ont. Fördelen är att myndighetsformen i välfinansierade tider säkerställer stabil finansiering och stöd, samt ställer krav på att upprätthålla en hög standard på forskning och

https://www.fysik.lu.se/om-oss/prefektbrev/prefektbrev-2025/prefektbrev-maj-2025 - 2025-08-23