Journal article
Cerebrospinal fluid levels of fatty acid–binding protein 3 are associated with likelihood of amyloidopathy in cognitively healthy individuals
K Dhiman, VL Villemagne, C Fowler, P Bourgeat, QX Li, S Collins, CC Rowe, CL Masters, D Ames, K Blennow, H Zetterberg, RN Martins, V Gupta
Alzheimer S and Dementia Diagnosis Assessment and Disease Monitoring | Published : 2022
DOI: 10.1002/dad2.12377
Abstract
Introduction: Fatty acid–binding protein 3 (FABP3) is a biomarker of neuronal membrane disruption, associated with lipid dyshomeostasis—a notable Alzheimer's disease (AD) pathophysiological change. We assessed the association of cerebrospinal fluid (CSF) FABP3 levels with brain amyloidosis and the likelihood/risk of developing amyloidopathy in cognitively healthy individuals. Methods: FABP3 levels were measured in CSF samples of cognitively healthy participants, > 60 years of age (n = 142), from the Australian Imaging, Biomarkers & Lifestyle Flagship Study of Ageing (AIBL). Results: FABP3 levels were positively associated with baseline brain amyloid beta (Aβ) load as measured by standardized..
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Awarded by Cooperative Research Centres, Australian Government Department of Industry
Funding Acknowledgements
The authors thank the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL) Study Group (www.aibl.csiro.au) and Edith Cowan University (ECU) and Deakin University. The AIBL is a collaboration between the Commonwealth Scientific and Industrial Research Organisation (CSIRO), ECU, The Florey Institute of Neuroscience and Mental Health (FINMH), National Ageing Research Institute (NARI), and Austin Health. It involves support from CogState Ltd., Hollywood Private Hospital, and Sir Charles Gairdner Hospital. The initial core funding of the study was facilitated by CSIRO. The study receives funding from the National Health and Medical Research Council (NHMRC), the Dementia Collaborative Research Centres program (DCRC2), the Cooperative Research Centre (CRC) for Mental Health, the Australian Alzheimer's Research Foundation, and Operational Infrastructure Support from the Government of Victoria. The authors also thank the participants for their assistance and commitment. KD also thanks ECU HDR (Higher degree by research) Scholarship. Veer Gupta is supported by NHMRC Boosting Dementia Research Leadership Fellowship #RM34909. KB is supported by the Swedish Research Council (#2017-00915), the Swedish Alzheimer Foundation (#AF-742881), Hjaernfonden, Sweden (#FO2017-0243), the Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement (#ALFGBG-715986), the European Union Joint Program for Neurodegenerative Disorders (JPND2019-466-236), and the Alzheimer's Association 2021 Zenith Award (ZEN-21-848495). HZ is a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018-02532), the European Research Council (#681712 and #101053962), Swedish State Support for Clinical Research (#ALFGBG-71320), the Alzheimer Drug Discovery Foun-dation (ADDF), USA (#201809-2016862), the AD Strategic Fund and the Alzheimer's Association (#ADSF-21-831376-C, #ADSF-21-831381-C, and #ADSF-21-831377-C), the Olav Thon Foundation, the Erling-Persson Family Foundation, Stiftelsen foer Gamla Tjaenar-innor, Hjaernfonden, Sweden (#FO2019-0228), the European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement No 860197 (MIRIADE), the European Union Joint Programme - Neurodegenerative Disease Research (JPND2021-00694), and the UK Dementia Research Institute at UCL (UKDRI-1003). SC receives an NHMRC Practitioner Fellowship (#APP1105784).