Inhibition of phospholipase A2 in rat brain modifies different membrane fluidity parameters in opposite ways

Schaeffer, Evelin L.; Skaf, Heni D.; Novaes, Barbara de A.; Silva, Emanuelle R. da; Martins, Beatriz Anastacia Dállia; Joaquim, Henrique; Gattaz, Wagner F.

doi:10.1016/j.pnpbp.2011.05.001

Cited by 22 publications

(20 citation statements)

References 45 publications

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“…On the other hand, in animal experiments inhibition of PLA2 impaired learning and spatial memory, similar signs occurring in the earliest phases of AD [179]. Additionally, PLA2 inhibition led to reduced fatty acyl chain flexibility, linking PLA2 with AD via altered membrane fluidity [180]. In line, membrane phospholipid metabolism has been described to be reduced in the prefrontal cortex of mildly and moderately demented AD patients [181].…”

Section: Reviewmentioning

confidence: 99%

Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Veitinger

Varga

Guterres

et al. 2014

acta neuropathol commun

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Peripheral biomarkers play an indispensable role in quick and reliable diagnoses of any kind of disease. With the population ageing, the number of people suffering from age-related diseases is expected to rise dramatically over the coming decades. In particular, all types of cognitive deficits, such as Alzheimer’s disease, will increase. Alzheimer’s disease is characterised mainly by coexistence of amyloid plaques and neurofibrillary tangles in brain. Reliable identification of such molecular characteristics antemortem, however, is problematic due to restricted availability of appropriate sample material and definitive diagnosis is only possible postmortem. Currently, the best molecular biomarkers available for antemortem diagnosis originate from cerebrospinal fluid. Though, this is not convenient for routine diagnosis because of the required invasive lumbar puncture. As a consequence, there is a growing demand for additional peripheral biomarkers in a more readily accessible sample material. Blood platelets, due to shared biochemical properties with neurons, can constitute an attractive alternative as discussed here. This review summarises potential platelet Alzheimer’s disease biomarkers, their role, implication, and alteration in the disease. For easy comparison of their performance, the Hedge effect size was calculated whenever data were available.

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Section: Reviewmentioning

confidence: 99%

Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Veitinger

Varga

Guterres

et al. 2014

acta neuropathol commun

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show abstract

“…On the other hand, n-3 PUFA withdrawal modulated the phosphorylation of glycogen-synthase kinase-3β and ERK1/2, predisposing more hippocampal neurons to damage in an in vitro oxygen and glucose deprivation model of ischemia (Moreira et al, 2010b). Along with this, a decrease in the release of PUFAs from cell membranes in the rat hippocampus, as a result of reduced phospholipase-A2 activity, caused alterations in membrane fluidity that could account for loss of spatial memory and cognitive impairment in Alzheimer’s disease (Schaeffer et al, 2011). However, the protective effects of n-3 PUFAs under certain conditions seemed to be limited to some of the members of this class of fatty acids.…”

Section: Cellular Roles Of Fatty Acids In the Nervous Systemmentioning

confidence: 99%

Fatting the brain: a brief of recent research

Hussain¹,

Schmitt²,

Loeffler³

et al. 2013

Front. Cell. Neurosci.

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Fatty acids are of paramount importance to all cells, since they provide energy, function as signaling molecules, and sustain structural integrity of cellular membranes. In the nervous system, where fatty acids are found in huge amounts, they participate in its development and maintenance throughout life. Growing evidence strongly indicates that fatty acids in their own right are also implicated in pathological conditions, including neurodegenerative diseases, mental disorders, stroke, and trauma. In this review, we focus on recent studies that demonstrate the relationships between fatty acids and function and dysfunction of the nervous system. Fatty acids stimulate gene expression and neuronal activity, boost synaptogenesis and neurogenesis, and prevent neuroinflammation and apoptosis. By doing so, they promote brain development, ameliorate cognitive functions, serve as anti-depressants and anti-convulsants, bestow protection against traumatic insults, and enhance repairing processes. On the other hand, unbalance between different fatty acid families or excess of some of them generate deleterious side effects, which limit the translatability of successful results in experimental settings into effective therapeutic strategies for humans. Despite these constraints, there exists realistic evidence to consider that nutritional therapies based on fatty acids can be of benefit to several currently incurable nervous system diseases.

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“…Alterations in the Chol/PL ratio homeostasis may cause an abnormal function and pathological process [19] . The increased Chol/PL ratio in this study confirms alterations in membrane organisation leading to decreased fluidity, low permeability, and altered stability and morphology [56] .…”

Section: Discussionmentioning

confidence: 99%

“…Neuronal membranes are mainly composed of 3 types of lipids, namely glycerophospholipids, phosphosphingolipids and cholesterol. The physicochemical properties such as stability, permeability and fluidity of neuronal membranes are influenced by glycerophospholipids [19] . It has been shown that alterations in lipid homeostasis results in the impairment of brain development and leads to many of the neurodegenerative diseases, including Alzheimer (AD), Parkinson, Niemann-Pick and Huntington diseases [20] .…”

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Dietary Selenium or Zinc Supplementation Restores Brain Lipid Composition and Membrane Fluidity in Protein-Undernourished Rats

Adebayo

Salau²,

Sandhir³

et al. 2016

Dev Neurosci

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Studies have shown that protein undernutrition (PU) modifies the membrane lipid composition in the intestine and liver, as well as in plasma and other areas. However, there is limited information on the effect of PU on synaptosomal membrane lipid composition and fluidity and the protective role of selenium (Se) and zinc (Zn), which is a major focus of the present study. For 10 weeks, rats were fed diets containing 16% casein, which constituted the adequate protein diet, or 5% casein, representing the PU diet. The animals were supplemented with Se and Zn at a concentration of 0.15 and 227 mg L^-1, respectively, in drinking water for 3 weeks. The results showed a significant increase in total lipids, glycolipids, triglycerides, cholesterol, and the cholesterol/phospholipid (Chol/PL) ratio, and a significant reduction in phospholipids and membrane fluidity. Se and Zn supplementation to PU rats, however, significantly lowered total lipids, glycolipids, triglycerides, cholesterol, and the Chol/PL ratio, while phospholipids and membrane fluidity were significantly restored. It is concluded that a perturbed lipid composition induced by PU affects the membrane structure and fluidity, which in turn influences membrane functions. The study suggests that Se and Zn supplementation might be beneficial in restoring the lipid dyshomeostasis associated with PU.

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Inhibition of phospholipase A2 in rat brain modifies different membrane fluidity parameters in opposite ways

Cited by 22 publications

References 45 publications

Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Platelets, a reliable source for peripheral Alzheimer’s disease biomarkers?

Fatting the brain: a brief of recent research

Dietary Selenium or Zinc Supplementation Restores Brain Lipid Composition and Membrane Fluidity in Protein-Undernourished Rats

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