Abstract
Arachidonic acid is the second polyunsaturated fatty acid in brain and the first one belonging to the ω-6 series. Dietary intakes of arachidonic are between 50 and 300 mg/day in western diets but they might be underestimated. Triglycerides from fat would provide similar amounts than phospholipids of lean meat. Alzheimer’s disease is an age-associated degenerative disease and a critical health concern worldwide. Amyloid-β peptide oligomers are presently recognized as the main and earliest agents of Alzheimer’s disease although their neurotoxicity requires the presence of tau protein. We and others established that the arachidonic-specific cytosolic phospholipase A2is critical for the amyloid-β peptide oligomer neurotoxicity. Then, we showed that an arachidonic acid-rich diet increases the mouse sensitivity to the amyloid-β peptide oligomer deleterious effect without major increase of arachidonic acid levels in brain. This suggests that dietary arachidonic acid can exert its effects in brain through peripheral modifications. Involvement of systemic sub-inflammation and gut-brain communications are discussed based on the recent literature. The various data suggest that dietary arachidonic acid should be taken into account in the design of preventive strategies against Alzheimer’s disease.
Highlights
While the influence of docosahexaenoic acid [DHA] in Alzheimer’s disease [AD] or other neurodegenerative diseases focused the interest of scientific and medical communities, few works were devoted to the role of arachidonic acid [ARA] in these diseases
We showed that an arachidonic acid-rich diet increases the mouse sensitivity to the amyloid-b peptide oligomer deleterious effect without major increase of arachidonic acid levels in brain
This suggests that dietary arachidonic acid can exert its effects in brain through peripheral modifications
Summary
While the influence of docosahexaenoic acid [DHA] in Alzheimer’s disease [AD] or other neurodegenerative diseases focused the interest of scientific and medical communities, few works were devoted to the role of arachidonic acid [ARA] in these diseases. Neuro-inflammation contributes to the AD early synaptic dysfunctions and the neuronal death in the late steps of the disease. ARA is putatively involved in AD through its role in synaptic signal and in inflammatory process and regulation of its brain levels could be a target in the fight against AD occurrence and progression. < 150 mg/day 139–168 mg/day 130–150 mg/day and the role of neuro-inflammation, we will present recent data about ARA contribution to AD mechanisms including ours. On this basis, we will propose some hypothesis on the ARAassociated mechanisms in AD
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