Figure 1 | Scientific Reports

Figure 1

From: Transcriptomic and glycomic analyses highlight pathway-specific glycosylation alterations unique to Alzheimer’s disease

Figure 1

Increased MGAT1 expression corroborated by a raised complex and reduced high-mannose N-glycans abundance in AD. (A) MGAT1 gene expression from RNA-seq across human brains with different diagnoses. Data presented as log2 count per million (log2CPM). Data from different studies were separated into blocks. Adjusted p-values were calculated based on all protein-coding genes. NS p-value > 0.05, *p-value < 0.05 but adjusted p-value > 0.05, **p-value < 0.05 and adjusted p-value < 0.05. ANOVA p-values were after the multiple testing correction over all protein-coding genes. DLPFC dorsolateral prefrontal cortex, FP frontal pole, IFG inferior frontal gyrus, STG superior temporal gyrus, PHG parahippocampal gyrus, TCX temporal cortex, CER cerebellum. NCI: no cognitive impairment, MCI mild cognitive impairment, AD Alzheimer’s disease, PA pathological aging, PSP progressive supranuclear palsy, Other other types of dementia. (B) qPCR confirmation of MGAT1 expression in the medial temporal cortex (MTC) of AD and control participants. (C) The abundance of N-glycan subtypes from N-glycomics in MTC of AD and control participants. (D) The abundance of two intermediate structures (Hex:5 HexNAc: 2, Hex:5 HexNAc: 3) from N-glycomics in MTC of AD and control participants. *p-value < 0.05. (E) A schematic of the MGAT1 function. Red/blue boxes: higher/lower in AD than control. Glycan symbol key: green circles, mannose (Man); blue squares, N-acetylglucosamine (GlcNAc).

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