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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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

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 - 2026-06-09

New editors & first call From 2022 we at the Department for Gender Studies in Lund have the privilege to take on the responsibility as editors for TGV (Tidskrift för genusvetenskap / “Journal for Gender Studies”). The journal is going through a process of change in several other ways as well: The current editorial group, in Uppsala, are working on the transfer of the journal from printed to digita

https://www.gender.lu.se/about-department-gender-studies/tidskrift-genusvetenskap - 2026-06-09

An ethnographic study of religious and social barriers encountered by LGBTQ+ people across diverse traditions of faith. Denna sida på svenska PI professor Mia Liinason FORTE (ID no 2021-01970)   While Sweden frequently is recognized as a secular and liberal country with a broad acceptance for same-sex relationships, contemporary research presents a contradictory situation for religious lgbtq+ peop

https://www.gender.lu.se/liveability-crossroad-religion-gender-and-sexuality - 2026-06-09

Find our latest publications in the research portal Find researchers, research outputs (e.g. publications), projects and units through Lund University research portal! The Division of Gender Studies' latest publications are available via the Lund University research portal, Lucris. You can also find our researchers and current projects via the research portal.Our latest publications in LucrisDo yo

https://www.gender.lu.se/research-0/research-results-and-publications - 2026-06-09

Amaranta Thompson, 2025, The Ontology and Epistemologies of a Plant: The cannabis community in Buenos Aires, Argentina, Media-Tryck. Onur Kilic, 2024, Lubunya Assemblages: Queer Networked Resistances in Turkey. Media-Tryck Esethu Monakali, 2024, Trans Masculine Geographies: On Navigating Urban Spaces and Negotiating Liveable Lives in Cape Town and Johannesburg, South Africa. Media-Tryck Jamie Wood

https://www.gender.lu.se/research-0/research-results-and-publications/dissertations - 2026-06-09

The Division of Gender Studies is a dynamic division that has expanded and developed its research profile since 1978. It has played a central role at Lund University in moving gender analysis from the margins in most disciplines to the centre of social and cultural analysis. Gender Studies is an interdisciplinary subject in the Department of Sociology at the Faculty of Social Sciences, Lund Univer

https://www.gender.lu.se/about-division-gender-studies - 2026-06-09

Research at the Division of Gender Studies Gender Studies at Lund University offers a critical and inspiring intellectual environment, where researchers are actively engaged in advancing gender studies as a discipline to explore, problematise and develop further analytical, methodological, and empirical insights into gender and social justice.We approach this from diverse and intersecting starting

https://www.gender.lu.se/research-0/our-research - 2026-06-09

Staff at the Department of Gender Studies In alphabetical order (by surname) Marco BacioPhD CandidateE-mail: marco [dot] bacio [at] genus [dot] lu [dot] sePhone: +46 046-222 97 74Room: 236Personal homepage     Goodman, Sara  Licentiate, Lecturer, Head of Department  E-mail: Sara [dot] Goodman [at] genus [dot] lu [dot] se (Sara[dot]Goodman[at]genus[dot]lu[dot]se)  Phone: +46 46-222 44 02  Room: 238

https://www.gender.lu.se/contact-information/all-staff - 2026-06-09