• Corpus ID: 91008639

Mobilisation de l'acide arachidonique et sensibilité au peptide ß-amyloïde

  title={Mobilisation de l'acide arachidonique et sensibilit{\'e} au peptide {\ss}-amylo{\"i}de},
  author={M{\'e}lanie Thomas},
La maladie d’Alzheimer (MA) est un probleme majeur de sante publique. Elle se traduit par des atteintes de la memoire reposant sur des dysfonctionnements synaptiques induits par les oligomeres de peptide s-amyloide (As). Ceux-ci activent la phospholipase A2 cytosolique (cPLA2) qui libere l’acide arachidonique (ARA) des phospholipides (PL) membranaires neuronaux. L’acyl-CoA synthetase 4 (ACSL4) peut limiter cette liberation en favorisant la reincorporation d’ARA dans les PL. Dans l’alimentation… 



Arachidonic acid downregulates acyl-CoA synthetase 4 expression by promoting its ubiquitination and proteasomal degradation[S]

It is shown that ACSL4 is intrinsically ubiquitinated and that AA treatment can enhance its ubiquitination and a novel substrate-induced posttranslational regulatory mechanism by which AA downregulates AC SL4 protein expression in hepatic cells is identified.

Deacylation and reacylation of neural membrane glycerophospholipids

The deacylation-reacylation cycle is an important mechanism responsible for the introduction of polyunsaturated fatty acids into neural membrane glycerophospholipids, and under pathological situations (ischemia), the overstimulation of phospholipase A2 results in a rapid generation and accumulation of free fatty acids including arachidonic acid, eicosanoids, and lipid peroxides.

Molecular Characterization of a Phospholipase D Generating Anandamide and Its Congeners*

It is confirmed that a specific phospholipase D is responsible for the generation of N-acylethanolamines including anandamide, strongly suggesting the physiological importance of lipid molecules of this class.

Neuronal protein trafficking associated with Alzheimer disease

  • B. Tang
  • Biology
    Cell adhesion & migration
  • 2009
Changes in post-Golgi membrane trafficking in aging neurons that may influence APP processing is particularly relevant to late-onset, idiopathic AD.

Long-chain Acyl-CoA Synthetase 6 Preferentially Promotes DHA Metabolism*

The data support the hypothesis that Acsl6 functions primarily in DHA metabolism, and that its overexpression increases DHA and AA internalization primarily during the first 24 h of neuronal differentiation to stimulate PL synthesis and enhance neurite outgrowth.