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. 2023 Jan;94(1):90-92.
doi: 10.1136/jnnp-2022-329663. Epub 2022 Aug 10.

Plasma GFAP in presymptomatic and symptomatic familial Alzheimer's disease: a longitudinal cohort study

Antoinette O'Connor #  1   2 , Emily Abel #  3   2 , Andrea Lessa Benedet #  4 , Teresa Poole #  3   5 , Nicholas Ashton  4   6   7   8 , Philip Simon John Weston  3 , Amanda J Heslegrave  2 , Natalie Ryan  3   2 , Suzie Barker  3 , James M Polke  9 , Kaj Blennow  4   10 , Henrik Zetterberg #  2   4   10 , Nick C Fox #  3   2
Affiliations

Plasma GFAP in presymptomatic and symptomatic familial Alzheimer's disease: a longitudinal cohort study

Antoinette O'Connor et al. J Neurol Neurosurg Psychiatry. 2023 Jan.
No abstract available

Keywords: alzheimer's disease; neurochemistry.

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Conflict of interest statement

Competing interests: HZ has served at scientific advisory boards and/or as a consultant for Abbvie, Alector, Annexon, Apellis, Artery Therapeutics, AZTherapies, CogRx, Denali, Eisai, Nervgen, Novo Nordisk, Pinteon Therapeutics, Red Abbey Labs, Passage Bio, Roche, Samumed, Siemens Healthineers, Triplet Therapeutics, and Wave, has given lectures in symposia sponsored by Cellectricon, Fujirebio, Alzecure, Biogen, and Roche, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program (outside submitted work). KB has served as a consultant, at advisory boards, or at data monitoring committees for Abcam, Axon, BioArctic, Biogen, JOMDD/Shimadzu. Julius Clinical, Lilly, MagQu, Novartis, Ono Pharma, Pharmatrophix, Prothena, Roche Diagnostics, and Siemens Healthineers, and is a cofounder of Brain Biomarker Solutions in Gothenburg AB (BBS), which is a part of the GU Ventures Incubator Program, outside the work presented in this paper. NCF has served on advisory boards or as a consultant for Biogen, Ionis, Lilly, and Roche (all payments to UCL) and has served on a data safety monitoring board for Biogen.

Figures

Figure 1
Figure 1
(A) Box plot for observed baseline plasma GFAP concentration. The measured plasma GFAP concentrations at baseline (first visit) are shown. Mutation carriers have been divided into those who are symptomatic (SMC) and those who are presymptomatic (PMC). The estimated geometric mean GFAP concentration in symptomatic carriers was 238% higher (95% CI 141% to 374%, p<0.001) than in non-carriers, and in presymptomatic carriers was 95% higher (95% CI 46% to 159%, p<0.001) than in non-carriers, after adjusting for age and sex. Age-and sex-adjusted geometric mean GFAP concentration was also significantly elevated in symptomatic compared with presymptomatic carriers (73% higher, 95% CI 26% to 138%, p=0.001). Boxes show the median and first and third quartiles. Dots represent individual observations. (B) Observed plasma GFAP concentration against estimated years to/from symptom onset. Symptomatic mutation carriers are shown in red, presymptomatic mutation carriers are shown in blue, non-carriers are shown in black. To preserve blinding to genetic status, all observed values for timepoints more than 19.3 years before expected symptom onset are shown in grey and some timepoints have been removed for at risk individuals. (C) Trajectory of plasma GFAP against estimated years to/from onset. Modelled geometric mean plasma against estimated years to/from symptom onset. Mutation carriers represented in red; non-carriers in black. Estimates are shown for a hypothetical male aged 41 years (the mean age at baseline). Dotted lines indicate 95% CIs. The y-axis scale is logarithmic in all panes. GFAP, glial fibrillar acidic protein.
See this image and copyright information in PMC

References

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