Beneficial Effects of Fish Oil on Human Brain

Farooqui, Akhlaq A.

doi:10.1007/978-1-4419-0543-7

Cited by 55 publications

(47 citation statements)

References 830 publications

(1,199 reference statements)

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“…In addition, non-enzymic lipid mediators (neuroprostanes, neuroketal, and neurofurans) of DHA metabolism may interact with NF-κB and facilitate the expression and release of inflammatory cytokines (Fig. 6), such as TNF-α, IL-β, and IL-6, which may further stimulate not only PlsEtn-PLA 2 activity but also other isoforms of PLA 2 including cPLA 2 and sPLA 2 [16]. Finally, ceramide also stimulates caspases cascade promoting apoptotic cell death (Fig.…”

Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

“…As stated above, plasmalogens represent between 1/2 and 2/3 of the ethanolamine phospholipids in the brain. During aging, the PlsEtn content in human brain are decreased [16]. Plasmalogens act as antioxidant [28,29].…”

Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

“…The loss of ethanolamine plasmalogen in neural membranes from AD patients may lead to neural membrane destabilization in several ways: (a) Plasmalogen deficiency may induce changes in the critical temperature necessary for maintaining the stability of lipid bilayer [16,21], and (b) the generation of lysoplasmalogen in neural membrane may induce changes in membrane fluidity and permeability and allow the influx of external Ca 2+ via plasma membrane channels [10]. Finally, the loss of plasmalogens also produces impairment of muscarinic cholinergic signals and abnormal β-amyloid precursor protein processing [22][23][24].…”

Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

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Studies on Plasmalogen-Selective Phospholipase A2 in Brain

Farooqui

2010

Mol Neurobiol

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Plasmalogen-selective phospholipase A(2) (PlsEtn-PLA(2)) has been purified from pig brain using multiple column chromatographic procedure. The purified enzyme migrates as a single band on polyacrylamide. It is stimulated by Triton X-100 and inhibited by sodium deoxycholate. Purified PlsEtn-PLA(2) is inhibited by iodoacetate, and this inhibition can be prevented by beta-meracaptoethanol. Treatment of neuronal cell cultures with kainic acid stimulates PlsEtn-PLA(2) activity in a dose-dependent manner, and this stimulation can be blocked by Ly294486, a selective kainic acid receptor antagonist. Activities of PlsEtn-PLA(2) are markedly increased in plasma membrane and synaptosomal plasma membrane fraction prepared from nucleus basalis and hippocampal region of brains from Alzheimer disease patients compared to age-matched controls. It is proposed that accumulation of ceramide and increased expression of cytokines may be responsible for the stimulation of PlsEtn-PLA(2) in Alzheimer disease.

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Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

Section: Activities Of Plasmalogen-selective Pla 2 In Alzheimer Diseasementioning

confidence: 99%

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Studies on Plasmalogen-Selective Phospholipase A2 in Brain

Farooqui

2010

Mol Neurobiol

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“…The Western diet, on the contrary, contains high amounts of ARA, palmitic and stearic acids. It is deficient in DHA and EPA [77]. The high intake of food enriched in ARA elevates levels of ARAderived eicosanoids and upregulates the expression of proinflammatory cytokines (TNF-a, and IL-1b).…”

Section: Lipid Mediators In Metabolic Syndrome and Neurological Disormentioning

confidence: 99%

“…Collective evidence suggests that levels of eicosanoids and docosanoids in brain and visceral tissues are partly regulated by diet [77]. Accumulation of saturated fatty acids in myocytes, hepatocytes, cardiomyocytes and pancreatic b cells, and the metabolic products of n-6 fatty acids have been linked to insulin resistance and metabolic syndrome [81].…”

Section: Lipid Mediators In Metabolic Syndrome and Neurological Disormentioning

confidence: 99%

Metabolic syndrome as a risk factor for neurological disorders

Farooqui

Panza

et al. 2011

Cell. Mol. Life Sci.

168

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The metabolic syndrome is a cluster of common pathologies: abdominal obesity linked to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. At the molecular level, metabolic syndrome is accompanied not only by dysregulation in the expression of adipokines (cytokines and chemokines), but also by alterations in levels of leptin, a peptide hormone released by white adipose tissue. These changes modulate immune response and inflammation that lead to alterations in the hypothalamic 'bodyweight/appetite/satiety set point,' resulting in the initiation and development of metabolic syndrome. Metabolic syndrome is a risk factor for neurological disorders such as stroke, depression and Alzheimer's disease. The molecular mechanism underlying the mirror relationship between metabolic syndrome and neurological disorders is not fully understood. However, it is becoming increasingly evident that all cellular and biochemical alterations observed in metabolic syndrome like impairment of endothelial cell function, abnormality in essential fatty acid metabolism and alterations in lipid mediators along with abnormal insulin/leptin signaling may represent a pathological bridge between metabolic syndrome and neurological disorders such as stroke, Alzheimer's disease and depression. The purpose of this review is not only to describe the involvement of brain in the pathogenesis of metabolic syndrome, but also to link the pathogenesis of metabolic syndrome with neurochemical changes in stroke, Alzheimer's disease and depression to a wider audience of neuroscientists with the hope that this discussion will initiate more studies on the relationship between metabolic syndrome and neurological disorders.

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Perspective and Directions for Future Studies

Farooqui

2011

Oxidative Stress in Vertebrates and Invertebrates

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Beneficial Effects of Fish Oil on Human Brain

Cited by 55 publications

References 830 publications

Studies on Plasmalogen-Selective Phospholipase A2 in Brain

Studies on Plasmalogen-Selective Phospholipase A2 in Brain

Metabolic syndrome as a risk factor for neurological disorders

Perspective and Directions for Future Studies

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