APOE ϵ4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer's disease

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Fältnamn	Indikatorer	Metadata
000		05322naa a2200649 4500
001		oai:gup.ub.gu.se/296422
003		SwePub
008		240910s2020 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:143860260
024	7	a https://gup.ub.gu.se/publication/2964222 URI
024	7	a https://doi.org/10.1186/s13195-020-00628-z2 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1438602602 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 Konijnenberg, E.4 aut
245	1 0	a APOE ϵ4 genotype-dependent cerebrospinal fluid proteomic signatures in Alzheimer's disease
264		c 2020-05-27
264	1	b Springer Science and Business Media LLC,c 2020
520		a Background: Aggregation of amyloid β into plaques in the brain is one of the earliest pathological events in Alzheimer's disease (AD). The exact pathophysiology leading to dementia is still uncertain, but the apolipoprotein E (APOE) ϵ4 genotype plays a major role. We aimed to identify the molecular pathways associated with amyloid β aggregation using cerebrospinal fluid (CSF) proteomics and to study the potential modifying effects of APOE ϵ4 genotype. Methods: We tested 243 proteins and protein fragments in CSF comparing 193 subjects with AD across the cognitive spectrum (65% APOE ϵ4 carriers, average age 75 ± 7 years) against 60 controls with normal CSF amyloid β, normal cognition, and no APOE ϵ4 allele (average age 75 ± 6 years). Results: One hundred twenty-nine proteins (53%) were associated with aggregated amyloid β. APOE ϵ4 carriers with AD showed altered concentrations of proteins involved in the complement pathway and glycolysis when cognition was normal and lower concentrations of proteins involved in synapse structure and function when cognitive impairment was moderately severe. APOE ϵ4 non-carriers with AD showed lower expression of proteins involved in synapse structure and function when cognition was normal and lower concentrations of proteins that were associated with complement and other inflammatory processes when cognitive impairment was mild. Repeating analyses for 114 proteins that were available in an independent EMIF-AD MBD dataset (n = 275) showed that 80% of the proteins showed group differences in a similar direction, but overall, 28% effects reached statistical significance (ranging between 6 and 87% depending on the disease stage and genotype), suggesting variable reproducibility. Conclusions: These results imply that AD pathophysiology depends on APOE genotype and that treatment for AD may need to be tailored according to APOE genotype and severity of the cognitive impairment. © 2020 The Author(s).
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
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Psykiatri0 (SwePub)302152 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Psychiatry0 (SwePub)302152 hsv//eng
653		a Amyloid aggregation
653		a APOE genotype
653		a CSF proteomics
700	1	a Tijms, B. M.4 aut
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 Dobricic, V.4 aut
700	1	a Bos, I.4 aut
700	1	a Vos, S.4 aut
700	1	a Tsolaki, M.4 aut
700	1	a Verhey, F.4 aut
700	1	a Popp, J.4 aut
700	1	a Martinez-Lage, P.4 aut
700	1	a Vandenberghe, R.4 aut
700	1	a Lleó, A.4 aut
700	1	a Frölich, L.4 aut
700	1	a Lovestone, S.4 aut
700	1	a Streffer, J.4 aut
700	1	a Bertram, L.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 Teunissen, C. E.4 aut
700	1	a Veerhuis, R.4 aut
700	1	a Smit, A. B.4 aut
700	1	a Scheltens, P.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 Alzheimer's Research and Therapyd : Springer Science and Business Media LLCg 12:1q 12:1x 1758-9193
856	4	u https://alzres.biomedcentral.com/track/pdf/10.1186/s13195-020-00628-z
856	4 8	u https://gup.ub.gu.se/publication/296422
856	4 8	u https://doi.org/10.1186/s13195-020-00628-z
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:143860260

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