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For patients

Petersén is head of the Huntington Disease Center and the clinical multi-professional HD team at the HD Clinic, located at the Neurology department at Skåne University Hospital (SUS) in Lund. The HD Center was formed at LU and Region Skåne with the aim to improve healthcare for families with HD and to bring research closer to the clinic. Please see www.huntingtoncentrum.se for more information. Th

https://www.huntington-research.lu.se/patients - 2025-07-03

Loss of the metabolism and sleep regulating neuronal populations expressing orexin and oxytocin in the hypothalamus in amyotrophic lateral sclerosis

Gabery S,  Ahmed RA, Caga J,  Kiernan MC, Halliday GM and Petersén Å. Neuropathology and Applied Neurobiology. 47(7): 979-989 (2021) doi.org/10.1111/nan.12709 Abstract Aims To determine the underlying cellular changes and clinical correlates associated with pathology of the hypothalamus in amyotrophic lateral sclerosis (ALS), as hypothalamic atrophy occurs in the preclinical phase of the disease.

https://www.huntington-research.lu.se/loss-metabolism-and-sleep-regulating-neuronal-populations-expressing-orexin-and-oxytocin - 2025-07-03

Effects of Deletion of Mutant Huntingtin in Steroidogenic Factor 1 Neurons on the Psychiatric and Metabolic Phenotype in the BACHD Mouse Model of Huntington Disease

Baldo B, Cheong RY, Petersén ÅPLoS One 9(10) (2014)AbstractPsychiatric and metabolic features appear several years before motor disturbances in the neurodegenerative Huntington’s disease (HD), caused by an expanded CAG repeat in the huntingtin (HTT) gene. Although the mechanisms leading to these aspects are unknown, dysfunction in the hypothalamus, a brain region controlling emotion and metabolism

https://www.huntington-research.lu.se/effects-deletion-mutant-huntingtin-steroidogenic-factor-1-neurons-psychiatric-and-metabolic - 2025-07-03

IKKβ signaling mediates metabolic changes in the hypothalamus of a Huntington’s disease mouse model

Soylu-Kucharz R, Khoshnan A and Petersén Å. bioRxiv 2021.04.08.438894; First published April 9, 2021. https://doi.org/10.1101/2021.04.08.438894 Abstract Background Huntington’s disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Metabolic changes are associated with HD progression, and underlying mechanisms are not fully known. As the IKKβ/NF

https://www.huntington-research.lu.se/ikkb-signaling-mediates-metabolic-changes-hypothalamus-huntingtons-disease-mouse-model - 2025-07-03

Effects of excitotoxicity in the hypothalamus in transgenic mouse models of Huntington disease

Henningsen JB,  Soylu-Kucharz R, Björkqvist M and Petersén Å. Heliyon. 2021 Aug 14;7(8):e07808. doi: 10.1016/j.heliyon.2021.e07808. eCollection 2021 Aug. Abstract Huntington disease (HD) is a fatal neurodegenerative movement disorder caused by an expanded CAG repeat in the huntingtin gene (HTT). The mutant huntingtin protein is ubiquitously expressed, but only certain brain regions are affected. T

https://www.huntington-research.lu.se/effects-excitotoxicity-hypothalamus-transgenic-mouse-models-huntington-disease - 2025-07-03

Cognitive symptoms and behavioural changes

Learn more from these short films where Åsa Petersén talks about cognitive symptoms and behavioural changes and psychiatric in Huntington's disease. Published by courtesy of Riksförbundet Huntingtons Sjukdom. All films are in Swedish. To view the Swedish subtitles, please click the button "CC" in the control bar (third from right) and choose "Svenska". Åsa Petersén about cognitive symptoms.   Åsa

https://www.huntington-research.lu.se/cognitive-symptoms-and-behavioural-changes - 2025-07-03

Early white matter pathology in the fornix of the limbic system in Huntington disease

Gabery S, Kwa JE, Cheong RY, Baldo B, Ferrari Bardile C, Tan B, McLean C, Georgiou-Karistianis N, Poudel GR, Halliday G, Pouladi MA and Petersén Å.  Acta Neuropathologica. 142(5): 791-806 (2021) doi: 10.1007/s00401-021-02362-8. Abstract Huntington disease (HD) is a fatal neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene. The typical motor symptoms have been a

https://www.huntington-research.lu.se/early-white-matter-pathology-fornix-limbic-system-huntington-disease - 2025-07-03

Ubiquitin specific protease-14 reduces cellular aggregates and protects against mutant huntingtin-induced cell degeneration: involvement of the proteasome and ER stress-activated kinase IRE1α

Hyrskyluoto A, Bruelle C, Lundh SH, Do HT, Kivinen J, Rappou E, Reijonen S, Waltimo T, Petersén Å, Lindholm D and Korhonen L.Human Molecular Genetics 23: 5928-5939 (2014)AbstractHuntington's disease (HD) is an autosomal inherited neurological disease caused by a CAG repeat expansion in the first exon of huntingtin gene encoding for the huntingtin protein (Htt). In HD there is an accumulation of in

https://www.huntington-research.lu.se/ubiquitin-specific-protease-14-reduces-cellular-aggregates-and-protects-against-mutant-huntingtin - 2025-07-03

Hypothalamic expression of huntingtin causes distinct metabolic changes in Huntington's disease mice

Dickson E, Soylu-Kucharz R , Petersén Å and Björkqvist M. Mol Metab. 2022 Mar;57:101439. doi: 10.1016/j.molmet.2022.101439. Epub 2022 Jan 7. Abstract Objective In Huntington's disease (HD), the disease-causing huntingtin (HTT) protein is ubiquitously expressed and causes both central and peripheral pathology. In clinical HD, a higher body mass index has been associated with slower disease progress

https://www.huntington-research.lu.se/hypothalamic-expression-huntingtin-causes-distinct-metabolic-changes-huntingtons-disease-mice - 2025-07-03

IKKβ signaling mediates metabolic changes in the hypothalamus of a Huntington's disease mouse model

Soylu-Kucharz R, Khoshnan A and Petersén Å. iScience 2022 Jan 19;25(2):103771. doi: 10.1016/j.isci.2022.103771. eCollection 2022 Feb 18. Abstract Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin (HTT) gene. Metabolic changes are associated with HD progression, but underlying mechanisms are not fully known. As the IKKβ/NF-κB pathway is an

https://www.huntington-research.lu.se/ikkb-signaling-mediates-metabolic-changes-hypothalamus-huntingtons-disease-mouse-model-0 - 2025-07-03

Microarray profiling of hypothalamic gene expression changes in Huntington’s disease mouse models

Dickson E, Sai Dwijesha A, Andersson N, Lundh S, Björkqvist M, Petersén Å and Soylu-Kucharz R. Frontiers in Neuroscience. 2022 Nov 3;16:1027269. doi: 10.3389/fnins.2022.1027269. PMID: 36408416; PMCID: PMC9671106. Abstract Structural changes and neuropathology in the hypothalamus have been suggested to contribute to the non-motor manifestations of Huntington’s disease (HD), a neurodegenerative diso

https://www.huntington-research.lu.se/microarray-profiling-hypothalamic-gene-expression-changes-huntingtons-disease-mouse-models - 2025-07-03

Twisting mice move the dystonia field forward

Petersén Å1 and Kirik D2.1Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund SE-221 84, Sweden.2Brain Repair and Imaging in Neural Systems (BRAINS) Unit, Department of Experimental Medical Science, Lund University, Lund SE-221 84, Sweden.Journal of Clinical Investigation 17:1-3 (2014)AbstractA common form of the hyperkinetic movement disor

https://www.huntington-research.lu.se/twisting-mice-move-dystonia-field-forward - 2025-07-03

Decreased CSF oxytocin relates to measures of social cognitive impairment in Huntington's disease patients

Hellem MNN, Cheong RY, Tonetto S, Vinther-Jensen T, Hendel RK, Larsen IU, Nielsen TT, Hjermind LE, Vogel A, Budtz-Jørgensen E, Petersén Å and Nielsen JE. Parkinsonism and Related Disorders. 99: 23-29 (2022).  Abstract Objective: Huntington's disease (HD) is an inherited neurodegenerative disease with motor, cognitive and psychiatric symptoms. Non-motor symptoms like depression and altered social c

https://www.huntington-research.lu.se/decreased-csf-oxytocin-relates-measures-social-cognitive-impairment-huntingtons-disease-patients - 2025-07-03

Oxytocin in Huntington’s disease and the spectrum of amyotrophic lateral sclerosis-frontotemporal dementia

Bergh S, Cheong R Y, Petersén Å and Gabery S. Front. Mol. Neurosci., 14 September 2022; Sec. Molecular Signalling and Pathways; doi.org/10.3389/fnmol.2022.984317   Abstract Neurodegenerative disorders (NDDs) such as Huntington’s disease (HD) and the spectrum of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are characterized by progressive loss of selectively vulnerable popu

https://www.huntington-research.lu.se/oxytocin-huntingtons-disease-and-spectrum-amyotrophic-lateral-sclerosis-frontotemporal-dementia - 2025-07-03

Comorbidities and clinical outcomes in adult- and juvenile-onset Huntington's disease: a study of linked Swedish National Registries (2002-2019)

Furby H, Moore S, Nordstroem A-L, Houghton R, Lambrelli D, Graham S, Svenningsson P and Petersén Å. Journal of Neurology. 270(2): 864-876 (2023) doi:10.1007/s00415-022-11418-y. Abstract Background: Huntington's disease (HD) is a rare, neurodegenerative disease and its complex motor, cognitive and psychiatric symptoms exert a lifelong clinical burden on both patients and their families. Objective:

https://www.huntington-research.lu.se/comorbidities-and-clinical-outcomes-adult-and-juvenile-onset-huntingtons-disease-study-linked - 2025-07-03

Publishing agreements and discounts

Through different types of publishing agreements, researchers at Lund University can publish open access with easier handling of the administrative processes and with negotiated costs. On this page you find out about what agreements you can use, and how. Publishing agreements for open access Through national agreements, negotiated by the National Library of Sweden, researchers at Lund University c

https://www.ub.lu.se/en/publish/open-access/publishing-agreements-and-discounts - 2025-07-03

Doctoral theses

REGISTER, PUBLISH AND MAKE YOUR DISSERTATION VISIBLE Here you find compiled information for doctoral students at Lund University about the procedure for registering, publishing and making their doctoral theses visible. Theses written at Lund University require ISBN number. Depending on which faculty and institution you belong to, you may order ISBN either from your faculty or from the University L

https://www.ub.lu.se/en/publish/doctoral-theses - 2025-07-03

Register and publish in full text

Registration in LUCRIS and adding a full text As a doctoral student at LU, you use LUCRIS to register your degree project and the thesis. The registration makes the thesis visible in LU's Research Portal and on the university's calendar for upcoming defenses. Also, make the theses freely available whenever possible. Register your doctoral thesis As a doctoral student at LU, you use LUCRIS to regis

https://www.ub.lu.se/en/publish/doctoral-theses/register-and-publish-thesis - 2025-07-03

Consortium with SND - Swedish National Data Service

Lund University has been a member of The SND Consortium, Swedish National Data Service, since 2018. The consortium includes seven universities and also has a network of twenty more additional universities. The consortium aims to build services for the description and publication of research data, based on, among other things, SND's existing supply and experience from almost 40 years of work in soc

https://www.ub.lu.se/en/publish/research-data/consortium-snd-swedish-national-data-service - 2025-07-03

AIP Publishing

Researchers at Lund University can use agreements to publish open access with easy handling of the administrative processes and negotiated costs. Read more about the terms of the agreement here. About the agreementThe agreement provides open access publishing under negotiated terms in 25 hybrid journals from AIP Publishing. Publishing in fully open-access journals is not included in the agreement.

https://www.ub.lu.se/en/publish/open-access/publishing-agreements-and-discounts/aip-publishing - 2025-07-03