Inhibition of GSK3β by pharmacological modulation of sphingolipid metabolism occurs independently of ganglioside disturbance in a cellular model of Alzheimer's disease

Noël, Anastasia; Ingrand, Sabrina; Barrier, Laurence

doi:10.1016/j.expneurol.2015.06.021

Cited by 4 publications

(3 citation statements)

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“…Many of these signaling pathways are closely associated with the occurrence and development of cognitive functions. Previous studies of signaling pathways are consistent with the GO and KEGG pathway analysis predictions in this present paper (43–51). For example, the sphingolipid signaling pathway was reported to play a role in AD and neurodegenerative diseases (43–45).…”

Section: Discussionsupporting

confidence: 92%

“…Previous studies of signaling pathways are consistent with the GO and KEGG pathway analysis predictions in this present paper (43–51). For example, the sphingolipid signaling pathway was reported to play a role in AD and neurodegenerative diseases (43–45). The FoxO signaling pathway has also been shown to be involved in the pathogenesis of AD (46).…”

Section: Discussionsupporting

confidence: 92%

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Abnormal expression of circRNA_089763 in the plasma exosomes of patients with post‑operative cognitive dysfunction after coronary artery bypass grafting

Wang

Liu

et al. 2019

Mol Med Report

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Post-operative cognitive dysfunction (POCD) is a complication of the central nervous system characterized by mental disorders, anxiety, personality changes and impaired memory. POCD occurs frequently after coronary artery bypass grafting (CABG) and can severely affect quality of life for patients. To date, the development of POCD biomarkers remains a challenge. Alterations in the expression of non-coding RNAs from brain tissue and peripheral blood have been linked to POCD. The present study aimed to detect the differential circular RNAs (circRNAs) in plasma exosomes of patients with POCD after CABG. The relative expression levels of circRNAs were analyzed using circRNA microarray analysis in the plasma exosomes of patients with POCD. Differentially altered circRNAs (P<0.05, fold change >1.5) were validated by reverse transcription-quantitative PCR in the plasma exosomes of patients with POCD. The target genes of the microRNAs were predicted using bioinformatics analysis. The functions and signaling pathways of these target genes were investigated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses. The microarray results indicated that the levels of nine circRNAs in patients with POCD were higher than those in the control subjects; and six circRNAs were at a lower level than those in control subjects. The RT-qPCR results from patients with POCD showed that only circRNA_089763 of the 15 circRNAs identified was significantly increased compared with control subjects. circRNA target gene prediction and functional annotation analysis showed significant enrichment in several GO terms and pathways associated with POCD. The present study provides evidence for the abnormal expression of POCD-induced circRNA_089763 in human plasma exosomes, as well as the involvement of POCD.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Abnormal expression of circRNA_089763 in the plasma exosomes of patients with post‑operative cognitive dysfunction after coronary artery bypass grafting

Wang

Liu

et al. 2019

Mol Med Report

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“…Four gangliosides - GM1, GD1a, GD1b and GT1b compose 96% of brain gangliosides. An altered ganglioside expression resulted in neural disorders, including seizures and axon degeneration1314. MAG, on the innermost wrap of the myelin sheath, binds to gangliosides GD1a and GT1b on axons with high affinity and to GM1 with moderate affinity.…”

mentioning

confidence: 99%

Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury

Rubovitch

Zilberstein

Chapman

et al. 2017

Sci Rep

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Blast induced traumatic brain injury (B-TBI) may cause various degrees of cognitive and behavioral disturbances but the exact brain pathophysiology involved is poorly understood. It was previously suggested that ganglioside alteration on the axon surface as well as axonal regenerating inhibitors (ARIs) such as myelin associated glycoprotein (MAG) were involved in axonal outgrowth inhibition (AOI), leading to brain damage. GM1 ganglioside content in the brain was significantly reduced while GD1 ganglioside was not affected. The axonal regeneration was also reduced as seen by the phosphorylated NF-H expression. Moreover, B-TBI induced a significant elevation in MAG expression in the brains of the injured mice. The blast injured mice exhibited a significant decline in spatial memory as seen by the Y-maze test. In addition, the injured mice showed pronounced damage to the visual memory (as evaluated by the Novel object recognition test). A single low dose of GM1 (2 mg/kg; IP), shortly after the injury, prevented both the cognitive and the cellular changes in the brains of the injured mice. These results enlighten part of the complicated mechanism that underlies the damage induced by B-TBI and may also suggest a potential new treatment strategy for brain injuries.

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Ganglioside and related-sphingolipid profiles are altered in a cellular model of Alzheimer's disease

2017

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Inhibition of GSK3β by pharmacological modulation of sphingolipid metabolism occurs independently of ganglioside disturbance in a cellular model of Alzheimer's disease

Cited by 4 publications

References 50 publications

Abnormal expression of circRNA_089763 in the plasma exosomes of patients with post‑operative cognitive dysfunction after coronary artery bypass grafting

Abnormal expression of circRNA_089763 in the plasma exosomes of patients with post‑operative cognitive dysfunction after coronary artery bypass grafting

Restoring GM1 ganglioside expression ameliorates axonal outgrowth inhibition and cognitive impairments induced by blast traumatic brain injury

Ganglioside and related-sphingolipid profiles are altered in a cellular model of Alzheimer's disease

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