Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer's disease: Associations with A beta-PET, neurodegeneration, and cognition

P. Chatterjee; L. Vermunt; B. Gordon; S. Pedrini; L. Boonkamp; N. Armstrong; C. Xiong; A. K. Singh; Y. Li; H. Sohrabi; K. Taddei; M.P. Molloy; T. L. S. Benzinger; J. Morris; C. Karch; S. Berman; J. Chhatwal; C. Cruchaga; N. Graff-Radford; Gregory S. Day; M. Farlow; N. Fox; A. Goate; J. Hassenstab; J-H Lee; J. Levin; E. McDade; H. Mori; R. Perrin; R. Sánchez-Valle; P. R. Schofield; A.I. Levey; M. Jucker; C. Masters; A. Fagan; R. Bateman; R. N. Martins; C. Teunissen

doi:10.1002/alz.12879

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Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer's disease: Associations with A beta-PET, neurodegeneration, and cognition

Journal article

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Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer's disease: Associations with A beta-PET, neurodegeneration, and cognition

P. Chatterjee, L. Vermunt, B. Gordon, S. Pedrini, L. Boonkamp, N. Armstrong, C. Xiong, A. K. Singh, Y. Li, H. Sohrabi, …

Alzheimer's & dementia, Vol.19(7), pp.2790-2804

2022

DOI: https://doi.org/10.1002/alz.12879

PMID: 36576155

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Abstract

Clinical Neurology

Life Sciences & Biomedicine

Neurosciences & Neurology

Science & Technology

Background: Glial fibrillary acidic protein (GFAP) is a promising candidate blood-based biomarker for Alzheimer's disease (AD) diagnosis and prognostication. The timing of its disease-associated changes, its clinical correlates, and biofluid-type dependency will influence its clinical utility. Methods: We evaluated plasma, serum, and cerebrospinal fluid (CSF) GFAP in families with autosomal dominant AD (ADAD), leveraging the predictable age at symptom onset to determine changes by stage of disease. Results: Plasma GFAP elevations appear a decade before expected symptom onset, after amyloid beta (A beta) accumulation and prior to neurodegeneration and cognitive decline. Plasma GFAP distinguished A beta-positive from A beta-negative ADAD participants and showed a stronger relationship with A beta load in asymptomatic than symptomatic ADAD. Higher plasma GFAP was associated with the degree and rate of neurodegeneration and cognitive impairment. Serum GFAP showed similar relationships, but these were less pronounced for CSF GFAP. Conclusion: Our findings support a role for plasma GFAP as a clinical biomarker of A beta-related astrocyte reactivity that is associated with cognitive decline and neurodegeneration.

Details

Title: Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer's disease: Associations with A beta-PET, neurodegeneration, and cognition
Authors/Creators: P. Chatterjee - Macquarie Univ, Macquarie Med Sch, 75 Talavera Rd, N Ryde, NSW 2109, Australia
L. Vermunt - Vrije Univ, Amsterdam Univ Med Ctr, Amsterdam Neurosci, Neurochem Lab,Dept Clin Chem, Amsterdam, Netherlands
B. Gordon - Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA
S. Pedrini - Edith Cowan Univ, Sarich Neurosci Res Inst, Sch Med Sci, Nedlands, WA, Australia
L. Boonkamp - Vrije Univ, Amsterdam Univ Med Ctr, Amsterdam Neurosci, Neurochem Lab,Dept Clin Chem, Amsterdam, Netherlands
N. Armstrong - Curtin Univ, Dept Math & Stat, Bentley, WA, Australia
C. Xiong - Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA
A. K. Singh - Macquarie Univ, Macquarie Business Sch, N Ryde, NSW, Australia
Y. Li - Washington Univ, Sch Med, Div Biostat, St Louis, MO USA
H. Sohrabi
K. Taddei - Edith Cowan Univ, Sarich Neurosci Res Inst, Sch Med Sci, Nedlands, WA, Australia
M.P. Molloy - Univ Sydney, Kolling Inst, Bowel Canc & Biomarker Lab, St Leonards, NSW, Australia
T. L. S. Benzinger - Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA
J. Morris - Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA
C. Karch - Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA
S. Berman - Univ Pittsburgh, Sch Med, Pittsburgh, PA USA
J. Chhatwal - Harvard Med Sch, Massachusetts Gen Hosp, Boston, MA 02115 USA
C. Cruchaga - Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA
N. Graff-Radford - Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA
Gregory S. Day - Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA
M. Farlow - Indiana Univ, Dept Neurol, Indianapolis, IN USA
N. Fox - UCL, Dementia Res Ctr, Queen Sq Inst Neurol, London, England
A. Goate - Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA
J. Hassenstab - Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA
J-H Lee - Univ Ulsan, Asan Med Ctr, Dept Neurol, Coll Med, Ulsan, South Korea
J. Levin - German Ctr Neurodegenerat Dis DZNE, Munich, Germany
E. McDade - Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA
H. Mori - Osaka Metropolitan Univ, Nagaoka Toku Univ, Osaka, Japan
R. Perrin - Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA
R. Sánchez-Valle - Hosp Clin Barcelona, Neurol Serv, Alzheimers Dis & Other Cognit Disorders Unit, Barcelona, Spain
P. R. Schofield - Neurosci Res Australia, Sydney, NSW, Australia
A.I. Levey - Emory Univ, Dept Neurol, Atlanta, GA USA
M. Jucker - German Ctr Neurodegenerat Dis DZNE, Tubingen, Germany
C. Masters - Florey Inst Neurosci & Mental Hlth, Melbourne, Vic, Australia
A. Fagan - Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA
R. Bateman - Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA
R. N. Martins - Macquarie Univ, Macquarie Med Sch, 75 Talavera Rd, N Ryde, NSW 2109, Australia
C. Teunissen - Vrije Univ, Amsterdam Univ Med Ctr, Amsterdam Neurosci, Neurochem Lab,Dept Clin Chem, Amsterdam, Netherlands
Publication Details: Alzheimer's & dementia, Vol.19(7), pp.2790-2804
Publisher: Wiley Periodicals LLC on behalf of Alzheimer's Association.
Identifiers: 991005548669307891
Murdoch Affiliation: Centre for Healthy Ageing
Language: English
Resource Type: Journal article

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Collaboration types: Domestic collaboration; International collaboration
Citation topics: 1 Clinical & Life Sciences; 1.52 Neurodegenerative Diseases; 1.52.60 Dementia
Web Of Science research areas: Clinical Neurology
ESI research areas: Neuroscience & Behavior