Dataset Information

Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

ABSTRACT: Vascular dementia is a transversal phenomenon in different kinds of neurodegenerative diseases involving acute and chronic brain alterations. Specifically, the role of phospholipids in the pathogenesis of dementia remains unknown. In the present study, we explored phospholipid profiles a month postischemia in cognitively impaired rats. The two-vessel occlusion (2-VO) model was used to generate brain parenchyma ischemia in adult male rats confirmed by alterations in myelin, endothelium, astrocytes and inflammation mediator. A lipidomic analysis was performed via mass spectrometry in the hippocampus and serum a month postischemia. We found decreases in phospholipids (PLs) associated with neurotransmission, such as phosphatidylcholine (PC 32:0, PC 34:2, PC 36:3, PC 36:4, and PC 42:1), and increases in PLs implied in membrane structure and signaling, such as lysophosphatidylethanolamine (LPE 18:1, 20:3, and 22:6) and phosphatidylserine (PS 38:4, 36:2, and 40:4), in the hippocampus. Complementarily, PC (PC 34:2, PC 34:3, PC 38:5, and PC 36:5) and ether-PC (ePC 34:1, 34:2, 36:2, 38:2, and 38:3) decreased, while Lyso-PC (LPC 18:0, 18:1, 20:4, 20:5, and LPC 22:6) and phosphatidylinositol (PI 36:2, 38:4, 38:5, and 40:5), as neurovascular state sensors, increased in the serum. Taken together, these data suggest inverse PC/LPC-PI levels as peripheral biomarkers and inverse PC/LPE-PS as a central indicator of postischemic cognitive impairment in rats.

SUBMITTER: Sabogal-Guaqueta AM

PROVIDER: S-EPMC6309919 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

Sabogal-Guáqueta Angelica Maria AM Villamil-Ortiz Javier Gustavo JG Arias-Londoño Julian David JD Cardona-Gómez Gloria Patricia GP

Frontiers in neuroscience 20181221

Vascular dementia is a transversal phenomenon in different kinds of neurodegenerative diseases involving acute and chronic brain alterations. Specifically, the role of phospholipids in the pathogenesis of dementia remains unknown. In the present study, we explored phospholipid profiles a month postischemia in cognitively impaired rats. The two-vessel occlusion (2-VO) model was used to generate brain parenchyma ischemia in adult male rats confirmed by alterations in myelin, endothelium, astrocyte ...[more]

PMID: 30627084

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Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.

Dataset Information

Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

Publications

Inverse Phosphatidylcholine/Phosphatidylinositol Levels as Peripheral Biomarkers and Phosphatidylcholine/Lysophosphatidylethanolamine-Phosphatidylserine as Hippocampal Indicator of Postischemic Cognitive Impairment in Rats.

Similar Datasets

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