Heterogeneity of the glial fibrillary acidic protein in gliosed human brains

1974 ◽  
Vol 23 (4) ◽  
pp. 551-563 ◽  
Author(s):  
D. Dahl ◽  
A. Bignami
2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Masayoshi Kano ◽  
Masashi Takanashi ◽  
Genko Oyama ◽  
Asako Yoritaka ◽  
Taku Hatano ◽  
...  

AbstractParkin (encoded by PRKN) is a ubiquitin ligase that plays an important role in cellular mitochondrial quality control. Mutations in PRKN cause selective dopaminergic cell loss in the substantia nigra and are presumed to induce a decrease in mitochondrial function caused by the defective clearance of mitochondria. Several studies have demonstrated that parkin dysfunction causes mitochondrial injury and astrocytic dysfunction. Using immunohistochemical methods, we analyzed astrocytic changes in human brains from individuals with PRKN mutations. Few glial fibrillary acidic protein- and vimentin-positive astrocytes were observed in the substantia nigra in PRKN-mutated subjects compared with subjects with idiopathic Parkinson’s disease. We also differentiated patient-specific induced pluripotent stem cells into midbrain organoids and confirmed decreased numbers of glial fibrillary acidic protein-positive astrocytes in PRKN-mutated organoids compared with age- and sex-matched controls. Our study reveals PRKN-mutation-induced astrocytic alteration and suggests the possibility of an astrocyte-related non-autonomous cell death mechanism for dopaminergic neurons in brains of PRKN-mutated patients.


Pathology ◽  
1983 ◽  
Vol 15 (4) ◽  
pp. 373-378 ◽  
Author(s):  
Stephen J. Lolait ◽  
J.H. Harmer ◽  
G. Auteri ◽  
J.S. Pedersen ◽  
B.H. Toh

2021 ◽  
Vol 10 (4) ◽  
pp. 662
Author(s):  
Eun-Hee Kim ◽  
Young-Eun Jang ◽  
Sang-Hwan Ji ◽  
Ji-Hyun Lee ◽  
Sung-Ae Cho ◽  
...  

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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