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ProgramThursday, May 7, 2026 | Skåne University Hospital Aula in Lund (Entrégatan 7)TimeSession8:45 – 9:00Name badge collection9:00 – 9:10Introduction by Martin Garwicz9:10 – 9:50Precision Prevention and Combination Therapies for Alzheimer’s Disease and Related DementiasProf. Miia Kivipelto (Karolinska Institutet)Chair: Niklas Mattsson-Carlgren9:50 – 10:20Coffee break10:20 – 11:00Next challenges i
https://www.neuroscience.lu.se/NSD2026-program - 2026-08-29
Neuroscience Day 2027 will provide an opportunity for students and researchers to showcase their work in an oral presentation format.Two stipends of 8,000 SEK will be awarded to the top two presenters.The deadline for abstract submission will be announced when registration opens for Neuroscience Day 2027.
https://www.neuroscience.lu.se/events/neuroscience-day/abstract-submission - 2026-08-29
Previously invited speakersNote: Years with links lead to the relevant event page in Lund University's Research Portal with information on that year's organizing committee. Segerfalk Lecturers who have been interviewed at Lund University are linked to the relevant article.2026Miia Kivipelto, Stockholm, SwedenLaia Montoliu-Gaya, Gothenburg, SwedenMackenzie Mathis, Lausanne, SwitzerlandGustav Nilson
https://www.neuroscience.lu.se/events/neuroscience-day/past-events - 2026-08-29
Please note that there is no Segerfalk Mini-Symposium planned for 2026. The next Segerfalk Mini-Symposium is planned to take place in 2027. If you are a researcher interested in hosting and organizing the next Segerfalk Mini-Symposium, please send a brief description of your proposal along with a budget outline (3-5 pages total) to Megg at megg [dot] garcia-ryde [at] med [dot] lu [dot] se (megg[do
https://www.neuroscience.lu.se/events/segerfalk-symposium - 2026-08-29
Lund University neuroscientists are at the forefront of one of the greatest challenges of our time - trying to understand how the brain works. Across disciplines, LU neuroscientists share the same goals: to make key discoveries about brain function, to train the next generation of scientists, and to translate discoveries from the laboratory towards clinical practice. Calendar Link to RSS More even
https://www.neuroscience.lu.se/lund-university-neuroscience - 2026-08-29
Siebzehnrübl FA, Raber KA, Urbach YK, Schulze-Krebs A, Canneva F, Moceri S, Habermeyer J, Achoui D, Gupta B, Steindler DA, Stephan M, Nguyen HP, Bonin M, Riess O, Bauer A, Aigner L, Couillard-Despres S, Paucar MA, Svenningsson P, Osmand A, Andreew A, Zabel C, Weiss A, Kuhn R, Moussaoui S, Blockx I, Van der Linden A, Cheong RY, Roybon L, Petersén Å and von Hörsten S.PNAS 115 (37) E8765-E8774 (2018)
Gisselsson D, Jonson T, Petersén Å, Strombeck B, Dal Cin P, Hoglund M, Mitelman F, Mertens F and Mandahl N.Proceedings of the National Academy of Sciences USA 98: 12683-12688 (2001)AbstractAlthough mechanisms for chromosomal instability in tumors have been described in animal and in vitro models, little is known about these processes in man. To explore cytogenetic evolution in human tumors, chromo
Petersén Å, Hansson O and Brundin P.In Swedish. Läkartidningen 50: 5756-5761 (2001)AbstractHuntingtons sjukdom är en av flera kända neurologiska sjukdomar som beror på en expanderad CAG-repetition. Symtomen karakteriseras av motoriska, psykiska och kognitiva störningar. Muterat huntingtin uttrycks i hela kroppen, och neurodegeneration och aggregering av det muterade proteinet huntingtin sker i bas
https://www.huntington-research.lu.se/huntingtons-sjukdom-annu-ett-galet-protein - 2026-08-29
Petersén Å, Castilho RF, Hansson O, Wieloch T and Brundin P.Brain Research 857: 20-29 (2000)AbstractDisruption of intracellular calcium homeostasis is thought to play a role in neurodegenerative disorders such as Huntington's disease (HD). To study different aspects of putative pathogenic mechanisms in HD, we aimed to establish an in vitro model of calcium-induced toxicity in striatal neurons. The
Mundt-Petersén U, Petersén Å, Emgård M, Dunnett SB and Brundin P.Experimental Neurology 164:112-120 (2000)AbstractIn transplants of embryonic striatal cells placed into the excitotoxically lesioned rat striatum (a model of Huntington's disease), as many as 60 to 90% of the grafted cells are believed to die. Caspase activation is part of a cascade of events that can lead to apoptosis. We investigat
https://www.huntington-research.lu.se/caspase-inhibition-increases-embryonic-striatal-graft-survival - 2026-08-29
Petersén Å, Hansson O, Emgård M and Brundin P.Cell Transplantation 9: 577-584 (2000)AbstractTransplantation of embryonic ventral mesencephalon is a potential therapy for patients with Parkinson's disease. As only around 5-10% of embryonic dopaminergic neurons survive grafting into the adult striatum, it is considered necessary to use multiple donor embryos. To increase the survival of the grafted
Brundin P, Karlsson J, Emgård M, Kaminski Schierle GS, Hansson O, Petersén Å and Castilho RF.Cell Transplantation 9: 179-195 (2000)AbstractNeural transplantation is developing into a therapeutic alternative in Parkinson's disease. A major limiting factor is that only 3-20% of grafted dopamine neurons survive the procedure. Recent advances regarding how and when the neurons die indicate that events
https://www.huntington-research.lu.se/improving-survival-grafted-dopaminergic-neurons-review-over-current-approaches - 2026-08-29
Hansson O, Petersén Å, Leist M, Nicotera P, Castilho RF and Brundin P.Proceedings of the National Academy of Sciences USA 96: 8727-8732 (1999)AbstractHuntington's disease (HD) is a hereditary neurodegenerative disorder presenting with chorea, dementia, and extensive striatal neuronal death. The mechanism through which the widely expressed mutant HD gene mediates a slowly progressing striatal neuro
Petersén Å, Emgård M and Brundin P.Brain Research Bulletin 50: 275-281 (1999)AbstractThe survival of grafted embryonic striatal tissue, dissected from the lateral ganglionic eminence, depends on the status of the host striatum. We found significantly larger volumes of surviving graft tissue and of striatal-like tissue (P-zone) within the graft, when the host striatum had been subjected to an excit
Petersén Å and Brundin P.Experimental Neurology 160: 402-412 (1999)AbstractCiliary neurotrophic factor (CNTF) has a protective effect on the striatum in animal models of Huntington's disease. However, the mechanism through which it exerts its effect is not clear. In this study, we show that there is a concentration-dependent direct protective effect of CNTF against N-methyl-D-aspartate-mediated ex
Petersén Å, Mani K and Brundin P.Experimental Neurology 157: 1-18 (1999)AbstractWe review recent advances regarding the pathogenesis of Huntington's disease (HD). This genetic neurodegenerative disorder is caused by an expanded CAG repeat in a gene coding for a protein, with unknown function, called huntingtin. There is selective death of striatal and cortical neurons. Both in patients and a trans
https://www.huntington-research.lu.se/recent-advances-pathogenesis-huntingtons-disease - 2026-08-29
Baldo B, Gabery S, Soylu-Kucharz R, Cheong RY, Henningsen JB, Englund E, McLean C, Kirik D, Halliday G and Petersén Å.Neuropathology and Applied Neurobiology 45 (4): 361-379 (2019)AbstractAIMS:Metabolic dysfunction is involved in modulating the disease process in Huntington disease (HD) but the underlying mechanisms are not known. The aim of this study was to investigate if the metabolic regulator
Brundin P, Petersén Å and Hansson O.Journal of Neurosurgery 90: 804-806 (1999)No abstract available; this is a letter to the editor.The letter
https://www.huntington-research.lu.se/graft-survival - 2026-08-29
Pircs K, Petri R, Madsen S, Brattås PL, Vuono R, Ottosson DR, St-Amour I, Hersbach BA, Matusiak-Brückner M, Lundh SH, Petersén Å, Déglon N, Hébert SS, Parmar M, Barker RA and Jakobsson J.Cell Reports 24(6): 1397-1406 (2018)AbstractMany neurodegenerative diseases are characterized by the presence of intracellular protein aggregates, resulting in alterations in autophagy. However, the consequences o
Fjalldal S, Follin C, Svärd D, Rylander L, Gabery S, Petersen Å, Van Westen D, Sundgren P, Bjorkman-Burtscher I, Lätt J, Ekman B, Johanson A and Erfurth EM.European Journal of Endocrinology 178 (6): 577-587 (2018)AbstractCONTEXT:Patients with craniopharyngioma (CP) and hypothalamic lesions (HL) have cognitive deficits. Which neural pathways are affected is unknown.OBJECTIVE:To determine whether th
