Cognitively unimpaired individuals with a low burden of A beta pathology have a distinct CSF biomarker profile

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Fältnamn	Indikatorer	Metadata
000		04921naa a2200685 4500
001		oai:gup.ub.gu.se/306949
003		SwePub
008		240528s2021 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://gup.ub.gu.se/publication/3069492 URI
024	7	a https://doi.org/10.1186/s13195-021-00863-y2 DOI
040		a (SwePub)gu
041		a eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Mila-Aloma, M.4 aut
245	1 0	a Cognitively unimpaired individuals with a low burden of A beta pathology have a distinct CSF biomarker profile
264		c 2021-07-27
264	1	b Springer Science and Business Media LLC,c 2021
520		a Background: Understanding the changes that occur in the transitional stage between absent and overt amyloid-beta (A beta) pathology within the Alzheimer's continuum is crucial to develop therapeutic and preventive strategies. The objective of this study is to test whether cognitively unimpaired individuals with a low burden of A beta pathology have a distinct CSF, structural, and functional neuroimaging biomarker profile. Methods: Cross-sectional study of 318 middle-aged, cognitively unimpaired individuals from the ALFA+ cohort. We measured CSF A beta 42/40, phosphorylated tau (p-tau), total tau (t-tau), neurofilament light (NfL), neurogranin, sTREM2, YKL40, GFAP, IL6, S100B, and alpha-synuclein. Participants also underwent cognitive assessments, APOE genotyping, structural MRI, [F-18]-FDG, and [F-18]-flutemetamol PET. To ensure the robustness of our results, we used three definitions of low burden of A beta pathology: (1) positive CSF A beta 42/40 and < 30 Centiloids in A beta PET, (2) positive CSF A beta 42/40 and negative A beta PET visual read, and (3) 20-40 Centiloid range in A beta PET. We tested CSF and neuroimaging biomarker differences between the low burden group and the corresponding A beta-negative group, adjusted by age and sex. Results: The prevalence and demographic characteristics of the low burden group differed between the three definitions. CSF p-tau and t-tau were increased in the low burden group compared to the A beta-negative in all definitions. CSF neurogranin was increased in the low burden group definitions 1 and 3, while CSF NfL was only increased in the low burden group definition 1. None of the defined low burden groups showed signs of atrophy or glucose hypometabolism. Instead, we found slight increases in cortical thickness and metabolism in definition 2. Conclusions: There are biologically meaningful A beta-downstream effects in individuals with a low burden of A beta pathology, while structural and functional changes are still subtle or absent. These findings support considering individuals with a low burden of A beta pathology for clinical trials.
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 Preclinical
653		a Alzheimer's disease
653		a CSF
653		a Biomarkers
653		a Subthreshold
653		a Cognitively unimpaired
653		a fluid amyloid-beta
653		a alzheimers-disease
653		a neurodegeneration
653		a definition
653		a deposition
653		a Neurosciences & Neurology
700	1	a Shekari, M.4 aut
700	1	a Salvado, G.4 aut
700	1	a Gispert, J. D.4 aut
700	1	a Arenaza-Urquijo, E. M.4 aut
700	1	a Operto, G.4 aut
700	1	a Falcon, C.4 aut
700	1	a Vilor-Tejedor, N.4 aut
700	1	a Grau-Rivera, O.4 aut
700	1	a Sala-Vila, A.4 aut
700	1	a Sanchez-Benavides, G.4 aut
700	1	a Gonzalez-de-Echavarri, J. M.4 aut
700	1	a Minguillon, C.4 aut
700	1	a Fauria, K.4 aut
700	1	a Ninerola-Baizan, A.4 aut
700	1	a Perissinotti, A.4 aut
700	1	a Simon, M.4 aut
700	1	a Kollmorgen, G.4 aut
700	1	a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xzethe
700	1	a Blennow, Kaj,d 1958u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xbleka
700	1	a Suarez-Calvet, M.4 aut
700	1	a Molinuevo, J. L.4 aut
710	2	a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi4 org
773	0	t Alzheimers Research & Therapyd : Springer Science and Business Media LLCg 13:1q 13:1x 1758-9193
856	4	u https://alzres.biomedcentral.com/track/pdf/10.1186/s13195-021-00863-y
856	4 8	u https://gup.ub.gu.se/publication/306949
856	4 8	u https://doi.org/10.1186/s13195-021-00863-y

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