Membrane lipids under norm and pathology

2021 ◽  
Vol 19 (1) ◽  
pp. 59-75
Author(s):  
Basheer Abdullah Marzoog ◽  
◽  
Tatyana Ivanovna Vlasova ◽  

Introduction. Lipid is an essential component of the cell and its organelles membrane. The uniqueness and selectivity of lipids to specific functions and asymmetry of lipid distribution in the organelle’s membrane give the cell ability of being highly qualified and specified. Aim. The paper provides a comprehensive review of membrane lipids in different tissues and organelles of the cell in norm and disease. Material and methods. The paper analyzed the present literature data on membrane lipids behavior in physiology and pathology. Analysis of the literature. The major structural and functional lipids of the cell membrane are phosphatidylcholine > phosphatidylethanolamine. The absence/deficiency or augmentation of a specific type of lipid results in serious defects and usually life-threatening with a permanent disability. The observations discussed here suggest, the lipid peroxidation severity depends on the membrane lipid composition of the cell. Some tissue cells can handle lipoperoxidation and protect themselves from the peroxidation damaging products better, while other cells cannot compensate. Therefore, some organs are highly sensitive to peroxidation and irreversible changes occur rapidly. Conclusion. To sum up, the understanding of lipid’s role in norm and disease is clinically crucial to evaluate a novel therapeutic target to treat many metabolic disorders such as metabolic syndrome and some lysosomal storage disorders via targeting specific new signaling pathways, lipid molecules, and enzymes.

2019 ◽  
Vol 61 (5) ◽  
pp. 636-654 ◽  
Author(s):  
Sara Grassi ◽  
Paola Giussani ◽  
Laura Mauri ◽  
Simona Prioni ◽  
Sandro Sonnino ◽  
...  

Lipid rafts are small, dynamic membrane areas characterized by the clustering of selected membrane lipids as the result of the spontaneous separation of glycolipids, sphingolipids, and cholesterol in a liquid-ordered phase. The exact dynamics underlying phase separation of membrane lipids in the complex biological membranes are still not fully understood. Nevertheless, alterations in the membrane lipid composition affect the lateral organization of molecules belonging to lipid rafts. Neural lipid rafts are found in brain cells, including neurons, astrocytes, and microglia, and are characterized by a high enrichment of specific lipids depending on the cell type. These lipid rafts seem to organize and determine the function of multiprotein complexes involved in several aspects of signal transduction, thus regulating the homeostasis of the brain. The progressive decline of brain performance along with physiological aging is at least in part associated with alterations in the composition and structure of neural lipid rafts. In addition, neurodegenerative conditions, such as lysosomal storage disorders, multiple sclerosis, and Parkinson’s, Huntington’s, and Alzheimer’s diseases, are frequently characterized by dysregulated lipid metabolism, which in turn affects the structure of lipid rafts. Several events underlying the pathogenesis of these diseases appear to depend on the altered composition of lipid rafts. Thus, the structure and function of lipid rafts play a central role in the pathogenesis of many common neurodegenerative diseases.


2020 ◽  
Vol 21 (18) ◽  
pp. 6881 ◽  
Author(s):  
Alex E. Ryckman ◽  
Inka Brockhausen ◽  
Jagdeep S. Walia

Glycosphingolipids (GSLs) are a specialized class of membrane lipids composed of a ceramide backbone and a carbohydrate-rich head group. GSLs populate lipid rafts of the cell membrane of eukaryotic cells, and serve important cellular functions including control of cell–cell signaling, signal transduction and cell recognition. Of the hundreds of unique GSL structures, anionic gangliosides are the most heavily implicated in the pathogenesis of lysosomal storage diseases (LSDs) such as Tay-Sachs and Sandhoff disease. Each LSD is characterized by the accumulation of GSLs in the lysosomes of neurons, which negatively interact with other intracellular molecules to culminate in cell death. In this review, we summarize the biosynthesis and degradation pathways of GSLs, discuss how aberrant GSL metabolism contributes to key features of LSD pathophysiology, draw parallels between LSDs and neurodegenerative proteinopathies such as Alzheimer’s and Parkinson’s disease and lastly, discuss possible therapies for patients.


2015 ◽  
Vol 35 (11) ◽  
pp. 1137-1147 ◽  
Author(s):  
Jyotsna Verma ◽  
Divya C. Thomas ◽  
Sandeepika Sharma ◽  
Geetu Jhingan ◽  
Renu Saxena ◽  
...  

Author(s):  
Sathiji Nageshwaran ◽  
Heather C Wilson ◽  
Anthony Dickenson ◽  
David Ledingham

This chapter discusses the clinical features and management of inborn errors of metabolism (lysosomal storage disorders, peroxisomal disorders, Wilson’s disease, porphyria, and phenylketonuria), vitamin and nutrient deficiency syndromes, and neurological toxicity syndromes.


Author(s):  
Daniel Erskine ◽  
David Koss ◽  
Viktor I. Korolchuk ◽  
Tiago F. Outeiro ◽  
Johannes Attems ◽  
...  

AbstractAccumulation of the protein α-synuclein into insoluble intracellular deposits termed Lewy bodies (LBs) is the characteristic neuropathological feature of LB diseases, such as Parkinson’s disease (PD), Parkinson’s disease dementia (PDD) and dementia with LB (DLB). α-Synuclein aggregation is thought to be a critical pathogenic event in the aetiology of LB disease, based on genetic analyses, fundamental studies using model systems, and the observation of LB pathology in post-mortem tissue. However, some monogenic disorders not traditionally characterised as synucleinopathies, such as lysosomal storage disorders, iron storage disorders and mitochondrial diseases, appear disproportionately vulnerable to the deposition of LBs, perhaps suggesting the process of LB formation may be a result of processes perturbed as a result of these conditions. The present review discusses biological pathways common to monogenic disorders associated with LB formation, identifying catabolic processes, particularly related to lipid homeostasis, autophagy and mitochondrial function, as processes that could contribute to LB formation. These findings are discussed in the context of known mediators of α-synuclein aggregation, highlighting the potential influence of impairments to these processes in the aetiology of LB formation.


2021 ◽  
Author(s):  
Maurizio Pieroni ◽  
Federico Pieruzzi ◽  
Renzo Mignani ◽  
Francesca Graziani ◽  
Iacopo Olivotto ◽  
...  

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