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Depletion of rabphilin 3A in a transgenic mouse model (R6/1) of Huntington's disease, a possible culprit in synaptic dysfunction

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 - 2025-07-21

The R6/2 transgenic mouse model of Huntington's disease develops diabetes due to deficient beta-cell mass and exocytosis

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 - 2025-07-21

mHTT Seeding Activity: A Marker of Disease Progression and Neurotoxicity in Models of Huntington's Disease

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 - 2025-07-21

Combining neuroprotective treatment of embryonic nigral donor tissue with mild hypothermia of the graft recipient

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 - 2025-07-21

Proteolysis of NR2B by calpain in the hippocampus of epileptic rats

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 - 2025-07-21

Reduction of GnRH and infertility in the R6/2 mouse model of Huntington’s disease

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 - 2025-07-21

Asialoerythropoetin is not effective in the R6/2 line of Huntington's disease mice

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 - 2025-07-21

Evidence for dysfunction of the nigrostriatal pathway in the R6/1 line of transgenic Huntington's disease mice

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 - 2025-07-21

Maintenance of susceptibility to neurodegeneration following intrastriatal injections of quinolinic acid in a new transgenic mouse model of Huntington's disease

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 - 2025-07-21

Huntington's Disease: the mystery unfolds?

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 - 2025-07-21

Mice transgenic for exon 1 of the Huntington's disease gene display reduced striatal sensitivity to neurotoxicity induced by dopamine and 6-hydroxydopamine

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 - 2025-07-21

Expanded CAG repeats in exon 1 of the Huntington's Disease gene stimulate dopamine-mediated striatal neuron autophagy and degeneration

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 - 2025-07-21

Brain-derived neurotrophic factor inhibits apoptosis and dopamine-induced free radical production in striatal neurons but does not prevent cell death

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 - 2025-07-21

Employment

Annual leave, leave of absence and sick leave Here you will find information on how to apply for annual leave, parental leave, how you do if you need to care for a sick child, register illness or take time off for another reason. You will also find routines for annual leave administration at the Department of Chemistry.  Introduction of new employees For new employees and guests who will work at t

https://kilu.lu.se/en/internal/employment - 2025-07-21

Guest lodgings

Kemicentrum has a number of apartments and corridor rooms that are rented out to visiting researchers, exchange students and international scholars. The rental and management of our guest lodgings is handled by the Administrative Unit at the Department of Chemistry.General information about our guest lodgings can be found on the Kemicentrum website: Lodgings- KemicentrumMore detailed information o

https://kilu.lu.se/en/internal/support-and-tools/guest-lodgings - 2025-07-21

Use of central email lists

Within the Department of Chemistry, email lists are an efficient way to quickly and easily reach many people. These lists are used for informing and communicating within our department, our divisions, and research groups. Examples of use include disseminating information about dissertations, seminars, information meetings, workshops, house updates, and other events, as well as for management commu

https://kilu.lu.se/en/internal/support-and-tools/communication/use-central-email-lists - 2025-07-21

Chemistry IT

In order for us to help you with your computer, other IT equipment, and software installations, we need to limit ourselves to certain standard models. As a government agency, we are also required to comply with laws and regulations. This means that we cannot use any programs as data can be stored on servers in third countries. Purchase of IT equipmentPlease contact the IT coordinator when you need

https://kilu.lu.se/en/internal/support-and-tools/chemistry-it - 2025-07-21

Mailing via central email lists, documentation and management

Do you have something you want to communicate internally within the Department of Chemistry via our central mailing lists? The Administrative Unit manages these lists. Information about our central email listsKILU - Department of Chemistry All: This mailing list reaches all employees of the department. The information shared here should be of the greatest importance to everyone in the department,

https://kilu.lu.se/en/internal/support-and-tools/communication/use-central-email-lists/mailing-central-email-lists-documentation-and-management - 2025-07-21

Communication channels

The Department of Chemistry has a range of channels that are used to disseminate information and communicate with our target groups, both internally and externally. Internal communicationBelow you will find some of our main internal channels and their uses. Internal communication at the department is mainly done through the following channels:Head of department newsletter Newsletter from the Head

https://kilu.lu.se/en/internal/support-and-tools/communication/communication-channels - 2025-07-21

Purchases over 100,000 SEK

If you want to buy something between 100,000 and 700,000 SEK and there are no frame contracts or local contracts, you need to conduct a direct procurement. All purchases exceeding 100,000 SEK also need to be documented in Lund University's document management system W3D3. Templates and a checklist are available in both Swedish and English to assist you. Points 1-9 describe how to proceed. 1. Calcu

https://kilu.lu.se/en/internal/support-and-tools/purchase/purchases-over-100000-sek - 2025-07-21