Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/25666
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dc.contributor.authorChatterjee, Pratishtha-
dc.contributor.authorPedrini, Steve-
dc.contributor.authorStoops, Erik-
dc.contributor.authorGoozee, Kathryn-
dc.contributor.authorVillemagne, Victor L-
dc.contributor.authorAsih, Prita R-
dc.contributor.authorVerberk, Inge M W-
dc.contributor.authorDave, Preeti-
dc.contributor.authorTaddei, Kevin-
dc.contributor.authorSohrabi, Hamid R-
dc.contributor.authorZetterberg, Henrik-
dc.contributor.authorBlennow, Kaj-
dc.contributor.authorTeunissen, Charlotte E-
dc.contributor.authorVanderstichele, Hugo M-
dc.contributor.authorMartins, Ralph N-
dc.date2021-
dc.date.accessioned2021-01-15T04:59:51Z-
dc.date.available2021-01-15T04:59:51Z-
dc.date.issued2021-01-11-
dc.identifier.citationTranslational Psychiatry 2021;11(1): 27en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/25666-
dc.description.abstractGlial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein, can be measured in blood samples, and has been associated with Alzheimer's disease (AD). However, plasma GFAP has not been investigated in cognitively normal older adults at risk of AD, based on brain amyloid-β (Aβ) load. Cross-sectional analyses were carried out for plasma GFAP and plasma Aβ1-42/Aβ1-40 ratio, a blood-based marker associated with brain Aβ load, in participants (65-90 years) categorised into low (Aβ-, n = 63) and high (Aβ+, n = 33) brain Aβ load groups via Aβ positron emission tomography. Plasma GFAP, Aβ1-42, and Aβ1-40 were measured using the Single molecule array (Simoa) platform. Plasma GFAP levels were significantly higher (p < 0.00001), and plasma Aβ1-42/Aβ1-40 ratios were significantly lower (p < 0.005), in Aβ+ participants compared to Aβ- participants, adjusted for covariates age, sex, and apolipoprotein E-ε4 carriage. A receiver operating characteristic curve based on a logistic regression of the same covariates, the base model, distinguished Aβ+ from Aβ- (area under the curve, AUC = 0.78), but was outperformed when plasma GFAP was added to the base model (AUC = 0.91) and further improved with plasma Aβ1-42/Aβ1-40 ratio (AUC = 0.92). The current findings demonstrate that plasma GFAP levels are elevated in cognitively normal older adults at risk of AD. These observations suggest that astrocytic damage or activation begins from the pre-symptomatic stage of AD and is associated with brain Aβ load. Observations from the present study highlight the potential of plasma GFAP to contribute to a diagnostic blood biomarker panel (along with plasma Aβ1-42/Aβ1-40 ratios) for cognitively normal older adults at risk of AD.en
dc.language.isoeng-
dc.subjectAlzheimer's diseaseen
dc.titlePlasma glial fibrillary acidic protein is elevated in cognitively normal older adults at risk of Alzheimer's disease.en
dc.typeJournal Articleen
dc.identifier.journaltitleTranslational Psychiatryen
dc.identifier.affiliationCentre for Healthy Ageing, School of Psychology and Exercise Science, College of Science, Health, Engineering and Education, Murdoch University, Murdoch, WA, Australiaen
dc.identifier.affiliationDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Swedenen
dc.identifier.affiliationClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Swedenen
dc.identifier.affiliationDepartment of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, United Kingdomen
dc.identifier.affiliationUK Dementia Research Institute at UCL, London, UKen
dc.identifier.affiliationDepartment of Biomedical Sciences, Macquarie University, North Ryde, NSW, Australiaen
dc.identifier.affiliationSchool of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australiaen
dc.identifier.affiliationKaRa Institute of Neurological Diseases, Macquarie Park, NSW, Australiaen
dc.identifier.affiliationAnglicare, Castle Hill Sydney, NSW, Australiaen
dc.identifier.affiliationSchool of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, WA, Australiaen
dc.identifier.affiliationThe Cooperative Research Centre for Mental Health, Carlton South, Australiaen
dc.identifier.affiliationAustralian Alzheimer's Research Foundation, Nedlands, WA, Australiaen
dc.identifier.affiliationADx NeuroSciences, Gent, Belgiumen
dc.identifier.affiliationMolecular Imaging and Therapyen
dc.identifier.affiliationNeurochemistry Laboratory, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam University Medical Centers, Amsterdam, Netherlandsen
dc.identifier.affiliationBiomarkable, Gent, Belgiumen
dc.identifier.doi10.1038/s41398-020-01137-1en
dc.type.contentTexten
dc.identifier.orcid0000-0003-4877-1958en
dc.identifier.orcid0000-0002-3573-1554en
dc.identifier.orcid0000-0003-0341-7445en
dc.identifier.orcid0000-0003-3930-4354en
dc.identifier.orcid0000-0002-1890-4193en
dc.identifier.orcid0000-0002-4828-9363en
dc.identifier.pubmedid33431793-
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