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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 05778naa a2200697 4500 | |
| 001 | oai:gup.ub.gu.se/302013 | |
| 003 | SwePub | |
| 008 | 240528s2020 | |||||||||||000 ||eng| | |
| 009 | oai:prod.swepub.kib.ki.se:145851712 | |
| 024 | 7 | a https://gup.ub.gu.se/publication/3020132 URI |
| 024 | 7 | a https://doi.org/10.1093/brain/awaa3252 DOI |
| 024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1458517122 URI |
| 040 | a (SwePub)gud (SwePub)ki | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Tijms, B. M.4 aut |
| 245 | 1 0 | a Pathophysiological subtypes of Alzheimer's disease based on cerebrospinal fluid proteomics |
| 264 | c 2020-11-18 | |
| 264 | 1 | b Oxford University Press (OUP),c 2020 |
| 520 | a Alzheimer's disease is biologically heterogeneous, and detailed understanding of the processes involved in patients is critical for development of treatments. CSF contains hundreds of proteins, with concentrations reflecting ongoing (patho)physiological processes. This provides the opportunity to study many biological processes at the same time in patients. We studied whether Alzheimer's disease biological subtypes can be detected in CSF proteomics using the dual clustering technique non-negative matrix factorization. In two independent cohorts (EMIF-AD MBD and ADNI) we found that 705 (77% of 911 tested) proteins differed between Alzheimer's disease (defined as having abnormal amyloid, n=425) and controls (defined as having normal CSF amyloid and tau and normal cognition, n=127). Using these proteins for data-driven clustering, we identified three robust pathophysiological Alzheimer's disease subtypes within each cohort showing (i) hyperplasticity and increased BACE1 levels; (ii) innate immune activation; and (iii) blood-brain barrier dysfunction with low BACE1 levels. In both cohorts, the majority of individuals were labelled as having subtype 1 (80, 36% in EMIF-AD MBD; 117, 59% in ADNI), 71 (32%) in EMIF-AD MBD and 41 (21%) in ADNI were labelled as subtype 2, and 72 (32%) in EMIF-AD MBD and 39 (20%) individuals in ADNI were labelled as subtype 3. Genetic analyses showed that all subtypes had an excess of genetic risk for Alzheimer's disease (all P>0.01). Additional pathological comparisons that were available for a subset in ADNI suggested that subtypes showed similar severity of Alzheimer's disease pathology, and did not differ in the frequencies of co-pathologies, providing further support that found subtypes truly reflect Alzheimer's disease heterogeneity. Compared to controls, all non-demented Alzheimer's disease individuals had increased risk of showing clinical progression (all P<0.01). Compared to subtype 1, subtype 2 showed faster clinical progression after correcting for age, sex, level of education and tau levels (hazard ratio = 2.5; 95% confidence interval = 1.2, 5.1; P=0.01), and subtype 3 at trend level (hazard ratio = 2.1; 95% confidence interval = 1.0, 4.4; P=0.06). Together, these results demonstrate the value of CSF proteomics in studying the biological heterogeneity in Alzheimer's disease patients, and suggest that subtypes may require tailored therapy. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng |
| 653 | a Alzheimer's disease | |
| 653 | a cerebrospinal fluid | |
| 653 | a proteomics | |
| 653 | a subtypes | |
| 653 | a Neurosciences & Neurology | |
| 700 | 1 | a Gobom, Johanu 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)xgobjo |
| 700 | 1 | a Reus, L.4 aut |
| 700 | 1 | a Jansen, I.4 aut |
| 700 | 1 | a Hong, S. J.4 aut |
| 700 | 1 | a Dobricic, V.4 aut |
| 700 | 1 | a Kilpert, F.4 aut |
| 700 | 1 | a ten Kate, M.4 aut |
| 700 | 1 | a Barkhof, F.4 aut |
| 700 | 1 | a Tsolaki, M.4 aut |
| 700 | 1 | a Verhey, F. R. J.4 aut |
| 700 | 1 | a Popp, J.u Karolinska Institutet4 aut |
| 700 | 1 | a Martinez-Lage, P.4 aut |
| 700 | 1 | a Vandenberghe, R.4 aut |
| 700 | 1 | a Lle, A.4 aut |
| 700 | 1 | a Molinuevo, J. L.4 aut |
| 700 | 1 | a Engelborghs, S.4 aut |
| 700 | 1 | a Bertram, L.4 aut |
| 700 | 1 | a Lovestone, S.4 aut |
| 700 | 1 | a Streffer, J.4 aut |
| 700 | 1 | a Vos, S.4 aut |
| 700 | 1 | a Bos, I.4 aut |
| 700 | 1 | 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 |
| 700 | 1 | a Scheltens, P.4 aut |
| 700 | 1 | a Teunissen, C. E.4 aut |
| 700 | 1 | 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 |
| 700 | 1 | a Visser, P. J.4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org |
| 773 | 0 | t Braind : Oxford University Press (OUP)g 143, s. 3776-3792q 143<3776-3792x 0006-8950x 1460-2156 |
| 856 | 4 | u https://academic.oup.com/brain/article-pdf/143/12/3776/36123503/awaa325.pdf |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/302013 |
| 856 | 4 8 | u https://doi.org/10.1093/brain/awaa325 |
| 856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:145851712 |
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