title: The essential role of lipids in Alzheimer's disease.
abstract: In the absence of efficient diagnostic and therapeutic tools, Alzheimer's disease (AD) is a major public health concern due to longer life expectancy in the Western countries. Although the precise cause of AD is still unknown, soluble beta-amyloid (Abeta) oligomers are considered the proximate effectors of the synaptic injury and neuronal death occurring in the early stages of AD. Abeta oligomers may directly interact with the synaptic membrane, leading to impairment of synaptic functions and subsequent signalling pathways triggering neurodegeneration. Therefore, membrane structure and lipid status should be considered determinant factors in Abeta-oligomer-induced synaptic and cell injuries, and therefore AD progression. Numerous epidemiological studies have highlighted close relationships between AD incidence and dietary patterns. Among the nutritional factors involved, lipids significantly influence AD pathogenesis. It is likely that maintenance of adequate membrane lipid content could prevent the production of Abeta peptide as well as its deleterious effects upon its interaction with synaptic membrane, thereby protecting neurons from Abeta-induced neurodegeneration. As major constituents of neuronal lipids, n-3 polyunsaturated fatty acids are of particular interest in the prevention of AD valuable diet ingredients whose neuroprotective properties could be essential for designing preventive nutrition-based strategies. In this review, we discuss the functional relevance of neuronal membrane features with respect to susceptibility to Abeta oligomers and AD pathogenesis, as well as the prospective capacities of lipids to prevent or to delay the disease.
authors.affiliation: Lipidomix, ENSAIA - INPL, Nancy-Université, France.
authors.forename: Sabrina
authors.initials: S
authors.lastname: Florent-Béchard
authors.forename: Cédric
authors.initials: C
authors.lastname: Desbène
authors.forename: Pierre
authors.initials: P
authors.lastname: Garcia
authors.forename: Ahmad
authors.initials: A
authors.lastname: Allouche
authors.forename: Ihsen
authors.initials: I
authors.lastname: Youssef
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Escanyé
authors.forename: Violette
authors.initials: V
authors.lastname: Koziel
authors.forename: Marine
authors.initials: M
authors.lastname: Hanse
authors.forename: Catherine
authors.initials: C
authors.lastname: Malaplate-Armand
authors.forename: Christophe
authors.initials: C
authors.lastname: Stenger
authors.forename: Badreddine
authors.initials: B
authors.lastname: Kriem
authors.forename: Frances T
authors.initials: FT
authors.lastname: Yen-Potin
authors.forename: Jean Luc
authors.initials: JL
authors.lastname: Olivier
authors.forename: Thierry
authors.initials: T
authors.lastname: Pillot
authors.forename: Thierry
authors.initials: T
authors.lastname: Oster
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D015525:Fatty Acids, Omega-3 / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism / Q000502:physiology*; D021962:Membrane Microdomains / Q000378:metabolism; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology
chemical_list: D016229:Amyloid beta-Peptides; D015525:Fatty Acids, Omega-3