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FältnamnIndikatorerMetadata
00005350naa a2200601 4500
001oai:gup.ub.gu.se/302654
003SwePub
008240528s2021 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/3026542 URI
0247 a https://doi.org/10.1186/s13195-021-00781-z2 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Grau-Rivera, O.4 aut
2451 0a Association of weight change with cerebrospinal fluid biomarkers and amyloid positron emission tomography in preclinical Alzheimer's disease
264 c 2021-02-17
264 1b Springer Science and Business Media LLC,c 2021
520 a BackgroundRecognizing clinical manifestations heralding the development of Alzheimer's disease (AD)-related cognitive impairment could improve the identification of individuals at higher risk of AD who may benefit from potential prevention strategies targeting preclinical population. We aim to characterize the association of body weight change with cognitive changes and AD biomarkers in cognitively unimpaired middle-aged adults.MethodsThis prospective cohort study included data from cognitively unimpaired adults from the ALFA study (n=2743), a research platform focused on preclinical AD. Cognitive and anthropometric data were collected at baseline between April 2013 and November 2014. Between October 2016 and February 2020, 450 participants were visited in the context of the nested ALFA+ study and underwent cerebrospinal fluid (CSF) extraction and acquisition of positron emission tomography images with [F-18]flutemetamol (FTM-PET). From these, 408 (90.1%) were included in the present study. We used data from two visits (average interval 4.1years) to compute rates of change in weight and cognitive performance. We tested associations between these variables and between weight change and categorical and continuous measures of CSF and neuroimaging AD biomarkers obtained at follow-up. We classified participants with CSF data according to the AT (amyloid, tau) system and assessed between-group differences in weight change.ResultsWeight loss predicted a higher likelihood of positive FTM-PET visual read (OR 1.27, 95% CI 1.00-1.61, p=0.049), abnormal CSF p-tau levels (OR 1.50, 95% CI 1.19-1.89, p=0.001), and an A+T+ profile (OR 1.64, 95% CI 1.25-2.20, p=0.001) and was greater among participants with an A+T+ profile (p<0.01) at follow-up. Weight change was positively associated with CSF A42/40 ratio (beta =0.099, p=0.032) and negatively associated with CSF p-tau (beta=-0.141, p=0.005), t-tau (beta=-0.147 p=0.004) and neurogranin levels (beta=-0.158, p=0.002). In stratified analyses, weight loss was significantly associated with higher t-tau, p-tau, neurofilament light, and neurogranin, as well as faster cognitive decline in A+ participants only.ConclusionsWeight loss predicts AD CSF and PET biomarker results and may occur downstream to amyloid-beta accumulation in preclinical AD, paralleling cognitive decline. Accordingly, it should be considered as an indicator of increased risk of AD-related cognitive impairment.Trial registrationNCT01835717, NCT02485730, NCT02685969.
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
653 a Alzheimer's disease
653 a Preclinical
653 a Cognitively unimpaired
653 a Weight loss
653 a Biomarkers
653 a Risk factors
653 a Neurosciences & Neurology
7001 a Navalpotro-Gomez, I.4 aut
7001 a Sanchez-Benavides, G.4 aut
7001 a Suarez-Calvet, M.4 aut
7001 a Mila-Aloma, M.4 aut
7001 a Arenaza-Urquijo, E. M.4 aut
7001 a Salvado, G.4 aut
7001 a Sala-Vila, A.4 aut
7001 a Shekari, M.4 aut
7001 a Gonzalez-de-Echavarri, J. M.4 aut
7001 a Minguillon, C.4 aut
7001 a Ninerola-Baizan, A.4 aut
7001 a Perissinotti, A.4 aut
7001 a Simon, M.4 aut
7001 a Kollmorgen, G.4 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
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 Gispert, J. D.4 aut
7001 a Molinuevo, J. L.4 aut
7001 a Alfa Study, Alfa Study4 aut
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
7730 t Alzheimer's Research & Therapyd : Springer Science and Business Media LLCg 13:1q 13:1x 1758-9193
8564 u https://alzres.biomedcentral.com/track/pdf/10.1186/s13195-021-00781-z
8564 8u https://gup.ub.gu.se/publication/302654
8564 8u https://doi.org/10.1186/s13195-021-00781-z

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