MRI Features and Evolution of Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy: A Retrospective Cross-sectional and Longitudinal Study‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬‬

2022 ◽  
pp. 103512
Author(s):  
Huiting Liao ◽  
Qianlan Chen ◽  
Min Zhang ◽  
Weiwei Chen
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein ◽  
Cross Sectional ◽  
Mri Features

scholarly journals Serum Glial Fibrillary Acidic Protein (GFAP) Is a Marker of Disease Severity in Frontotemporal Lobar Degeneration

2020 ◽  
Vol 77 (3) ◽  
pp. 1129-1141 ◽  
Author(s):  
Alberto Benussi ◽  
Nicholas J. Ashton ◽  
Thomas K. Karikari ◽  
Stefano Gazzina ◽  
Enrico Premi ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Disease Severity ◽  
Single Molecule ◽  
Frontotemporal Lobar Degeneration ◽  
Acidic Protein ◽  
Cross Sectional ◽  
Indirect Measures ◽  
Neurophysiological Data ◽  
Diagnostic And Prognostic Value

Background: It is still unknown if serum glial fibrillary acidic protein (GFAP) is a useful marker in frontotemporal lobar degeneration (FTLD). Objective: To assess the diagnostic and prognostic value of serum GFAP in a large cohort of patients with FTLD. Methods: In this retrospective study, performed on 406 participants, we measured serum GFAP concentration with an ultrasensitive Single molecule array (Simoa) method in patients with FTLD, Alzheimer’s disease (AD), and in cognitively unimpaired elderly controls. We assessed the role of GFAP as marker of disease severity by analyzing the correlation with clinical variables, neurophysiological data, and cross-sectional brain imaging. Moreover, we evaluated the role of serum GFAP as a prognostic marker of disease survival. Results: We observed significantly higher levels of serum GFAP in patients with FTLD syndromes, except progressive supranuclear palsy, compared with healthy controls, but not compared with AD patients. In FTLD, serum GFAP levels correlated with measures of cognitive dysfunction and disease severity, and were associated with indirect measures of GABAergic deficit. Serum GFAP concentration was not a significant predictor of survival. Conclusion: Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD.

scholarly journals MRI diagnosis of Alexander disease

2012 ◽  
Vol 16 (3) ◽  
pp. 116-117 ◽  
Author(s):  
C G Muralidharan ◽  
R P S Tomar ◽  
R Aggarwal
Keyword(s):  
White Matter ◽  
Glial Fibrillary Acidic Protein ◽  
Missense Mutation ◽  
Alexander Disease ◽  
Acidic Protein ◽  
White Matter Abnormalities ◽  
Mri Features ◽  
Mri Diagnosis

Alexander disease (fibrinoid leucodystrophy; originally described by Alexander in 1949) is a rare, fatal, nonfamilial leucoencephalopathy caused by astrocyte dysfunction characterised by missense mutation in the genes coding for glial fibrillary acidic protein(GFAP). It typically presents with frontal preponderance of white matter abnormalities and macroencephaly. We report a case of leucoencephalopathy with macroencephaly that shows characteristic MRI features of Alexander disease.

Expression of glial fibrillary acidic protein, actin, fibronectin and factor VIII antigen in human astrocytomas

Pathology ◽  
1983 ◽  
Vol 15 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Stephen J. Lolait ◽  
J.H. Harmer ◽  
G. Auteri ◽  
J.S. Pedersen ◽  
B.H. Toh
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Factor Viii ◽  
Acidic Protein ◽  
Factor Viii Antigen ◽  
Human Astrocytomas

scholarly journals Changes in Plasma Glial Fibrillary Acidic Protein in Children Receiving Sevoflurane Anesthesia: A Preliminary Randomized Trial

2021 ◽  
Vol 10 (4) ◽  
pp. 662
Author(s):  
Eun-Hee Kim ◽  
Young-Eun Jang ◽  
Sang-Hwan Ji ◽  
Ji-Hyun Lee ◽  
Sung-Ae Cho ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Randomized Trial ◽  
Protein Concentration ◽  
Pediatric Patients ◽  
Neuronal Injury ◽  
Acidic Protein ◽  
Anesthesia Induction ◽  
Sevoflurane Anesthesia ◽  
Control Groups ◽  
Over Time

We investigated changes in plasma glial fibrillary acidic protein concentration during sevoflurane anesthesia induction in children < 3 years old and determined the effect of co-administering dexmedetomidine. This preliminary randomized trial included 60 pediatric patients who received sevoflurane anesthesia for >3 h. Patients were assigned to dexmedetomidine or control groups at a 1:1 ratio. The primary outcome was changes in plasma glial fibrillary acidic protein concentration of dexmedetomidine and control groups over time. Fifty-five patients were included in the final analysis. The median (interquartile range (IQR)) of the plasma glial fibrillary acidic protein level was 387.7 (298.9–510.8) pg·mL−1 immediately after anesthetic induction, 302.6 (250.9–412.5) pg·mL−1 at 30 min, and 321.9 (233.8–576.2) pg·mL−1 at 180 min after the first sample. These values did not change over time (p = 0.759). However, plasma glial fibrillary acidic protein increased after 180 min of infusion of dexmedetomidine compared with values at 30 min infusion (p = 0.04, mean difference and 95% confidence interval of 221.6 and 2.2 to 441.0 pg·mL−1). In conclusion, three hours of sevoflurane anesthesia in pediatric patients < 3 years old did not provoke neuronal injury assessed by the plasma biomarker. Further studies regarding the effect of prolonged dexmedetomidine infusion on anesthetic neuronal injury are required.

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