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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004444naa a2200649 4500
001oai:DiVA.org:umu-202430
003SwePub
008230109s2022 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-2024302 URI
0247 a https://doi.org/10.1002/mds.289322 DOI
040 a (SwePub)umu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Szwedo, Aleksandra A4 aut
2451 0a GBA and APOE impact cognitive decline in Parkinson's disease :b A 10-year population-based study
264 c 2022-02-02
264 1b John Wiley & Sons,c 2022
338 a electronic2 rdacarrier
520 a BACKGROUND: Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results.OBJECTIVES: To evaluate the effect of genetic variants in APOE, GBA, MAPT, and SNCA on cognitive decline and risk of dementia in a pooled analysis of six longitudinal, non-selective, population-based cohorts of newly diagnosed PD patients.METHODS: 1002 PD patients, followed for up to 10 years (median 7.2 years), were genotyped for at least one of APOE-ε4, GBA mutations, MAPT H1/H2, or SNCA rs356219. We evaluated the effect of genotype on the rate of cognitive decline (Mini-Mental State Examanation, MMSE) using linear mixed models and the development of dementia (diagnosed using standardized criteria) using Cox regression; multiple comparisons were accounted for using Benjamini-Hochberg corrections.RESULTS: Carriers of APOE-ε4 (n = 281, 29.7%) and GBA mutations (n = 100, 10.3%) had faster cognitive decline and were at higher risk of progression to dementia (APOE-ε4, HR 3.57, P < 0.001; GBA mutations, HR 1.76, P = 0.001) than non-carriers. The risk of cognitive decline and dementia (HR 5.19, P < 0.001) was further increased in carriers of both risk genotypes (n = 23). No significant effects were observed for MAPT or SNCA rs356219.CONCLUSIONS: GBA and APOE genotyping could improve the prediction of cognitive decline in PD, which is important to inform the clinical trial selection and potentially to enable personalized treatment © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
653 a APOE
653 a GBA
653 a Parkinson's disease
653 a cognitive decline
653 a dementia
653 a Human Anatomy
653 a anatomi
653 a nanomaterials
653 a nanomaterial
7001 a Dalen, Ingvild4 aut
7001 a Pedersen, Kenn Freddy4 aut
7001 a Camacho, Marta4 aut
7001 a Bäckström, David C,c M.D.d 1978-u Umeå universitet,Neurovetenskaper,Department of Neurology, and Department of Neuroscience, Yale University School of Medicine, New Haven, Connecticut, USA4 aut0 (Swepub:umu)dadbam02
7001 a Forsgren, Larsu Umeå universitet,Neurovetenskaper4 aut0 (Swepub:umu)lafo0001
7001 a Tzoulis, Charalampos4 aut
7001 a Winder-Rhodes, Sophie4 aut
7001 a Hudson, Gavin4 aut
7001 a Liu, Ganqiang4 aut
7001 a Scherzer, Clemens R4 aut
7001 a Lawson, Rachael A4 aut
7001 a Yarnall, Alison J4 aut
7001 a Williams-Gray, Caroline H4 aut
7001 a Macleod, Angus D4 aut
7001 a Counsell, Carl E4 aut
7001 a Tysnes, Ole-Bjørn4 aut
7001 a Alves, Guido4 aut
7001 a Maple-Grødem, Jodi4 aut
7102 a Umeå universitetb Neurovetenskaper4 org
7730 t Movement Disordersd : John Wiley & Sonsg 37:5, s. 1016-1027q 37:5<1016-1027x 0885-3185x 1531-8257
8564 u https://doi.org/10.1002/mds.28932y Fulltext
8564 u https://umu.diva-portal.org/smash/get/diva2:1724886/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/mds.28932
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-202430
8564 8u https://doi.org/10.1002/mds.28932

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