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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00007062naa a2200565 4500
001oai:gup.ub.gu.se/222692
003SwePub
008240528s2015 | |||||||||||000 ||eng|
009oai:lup.lub.lu.se:92d6afad-65c9-46c9-9309-e0b1431c4ec0
009oai:prod.swepub.kib.ki.se:131996407
0247 a https://gup.ub.gu.se/publication/2226922 URI
0247 a https://doi.org/10.1093/brain/awv1812 DOI
0247 a https://lup.lub.lu.se/record/77511052 URI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1319964072 URI
040 a (SwePub)gud (SwePub)lud (SwePub)ki
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Skillbäck, Tobiasu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xskito
2451 0a Cerebrospinal fluid tau and amyloid-β1-42 in patients with dementia.
264 c 2015-06-30
264 1b Oxford University Press (OUP),c 2015
520 a Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease. However, several neurodegenerative disorders may overlap with Alzheimer's disease both in regards to clinical symptoms and neuropathology. In a uniquely large cohort of dementia patients, we examined the associations of cerebrospinal fluid biomarkers for Alzheimer's disease molecular pathology with clinical dementia diagnoses and disease severity. We cross-referenced the Swedish Dementia Registry with the clinical laboratory database at the Sahlgrenska University Hospital. The final data set consisted of 5676 unique subjects with a clinical dementia diagnosis and a complete set of measurements for cerebrospinal fluid amyloid-β1-42, total tau and phosphorylated tau. In cluster analysis, disregarding clinical diagnosis, the optimal natural separation of this data set was into two clusters, with the majority of patients with early onset Alzheimer's disease (75%) and late onset Alzheimer's disease (73%) assigned to one cluster and the patients with vascular dementia (91%), frontotemporal dementia (94%), Parkinson's disease dementia (94%) and dementia with Lewy bodies (87%) to the other cluster. Frontotemporal dementia had the highest cerebrospinal fluid levels of amyloid-β1-42 and the lowest levels of total tau and phosphorylated tau. The highest levels of total tau and phosphorylated tau and the lowest levels of amyloid-β1-42 and amyloid-β1-42:phosphorylated tau ratios were found in Alzheimer's disease. Low amyloid-β1-42, high total tau and high phosphorylated tau correlated with low Mini-Mental State Examination scores in Alzheimer's disease. In Parkinson's disease dementia and vascular dementia low cerebrospinal fluid amyloid-β1-42 was associated with low Mini-Mental State Examination score. In the vascular dementia, frontotemporal dementia, dementia with Lewy bodies and Parkinson's disease dementia groups 53%, 34%, 67% and 53% of the subjects, respectively had abnormal amyloid-β1-42 levels, 41%, 41%, 28% and 28% had abnormal total tau levels, and 29%, 28%, 25% and 19% had abnormal phosphorylated tau levels. Cerebrospinal fluid biomarkers were strongly associated with specific clinical dementia diagnoses with Alzheimer's disease and frontotemporal dementia showing the greatest difference in biomarker levels. In addition, cerebrospinal fluid amyloid-β1-42, total tau, phosphorylated tau and the amyloid-β1-42:phosphorylated tau ratio all correlated with poor cognitive performance in Alzheimer's disease, as did cerebrospinal fluid amyloid-β1-42 in Parkinson's disease dementia and vascular dementia. The results support the use of cerebrospinal fluid biomarkers to differentiate between dementias in clinical practice, and to estimate disease severity.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
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
7001 a Farahmand, Bahman Y4 aut
7001 a Rosén, Christoffer,d 1986u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xrochr
7001 a Mattsson, Niklas,d 1979u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xmattn
7001 a Nägga, Katarinau Lund University,Lunds universitet,Klinisk minnesforskning,Forskargrupper vid Lunds universitet,Clinical Memory Research,Lund University Research Groups4 aut0 (Swepub:lu)med-kng
7001 a Kilander, Lena4 aut
7001 a Religa, Dorotau Karolinska Institutet4 aut
7001 a Wimo, Andersu Karolinska Institutet4 aut
7001 a Winblad, Bengtu Karolinska Institutet4 aut
7001 a Schott, Jonathan M4 aut
7001 a Blennow, Kaj,d 1958u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xbleka
7001 a Eriksdotter, Mariau Karolinska Institutet4 aut
7001 a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xzethe
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
7730 t Brain : a journal of neurologyd : Oxford University Press (OUP)g 138:Pt 9, s. 2716-31q 138:Pt 9<2716-31x 1460-2156x 0006-8950
7730 t Braind : Oxford University Press (OUP)g 138:Pt 9, s. 2716-31q 138:Pt 9<2716-31x 0006-8950
8564 u https://academic.oup.com/brain/article-pdf/138/9/2716/13800222/awv181.pdf
8564 u http://www.ncbi.nlm.nih.gov/pubmed/26133663?dopt=Abstracty FULLTEXT
8564 u http://dx.doi.org/10.1093/brain/awv181y FULLTEXT
8564 8u https://gup.ub.gu.se/publication/222692
8564 8u https://doi.org/10.1093/brain/awv181
8564 8u https://lup.lub.lu.se/record/7751105
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:131996407

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