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Article type: Research Article
Authors: Iuliano, Luigia | Pacelli, Antonioa | Ciacciarelli, Marcoa | Zerbinati, Chiaraa | Fagioli, Sabrinab | Piras, Fabriziob | Orfei, Maria Donatab | Bossù, Paolab | Pazzelli, Florianab; e | Serviddio, Gaetanod | Caltagirone, Carlob; c | Spalletta, Gianfrancob
Affiliations: [a] Department of Medico-Surgical Sciences and Biotechnology, Vascular Biology and Mass Spectrometry Laboratory, Sapienza University of Rome, Latina, Italy | [b] Laboratory of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy | [c] Department of Neuroscience, Tor Vergata University of Rome, Rome, Italy | [d] Institute of Internal Medicine, University of Foggia, Foggia, Italy | [e] NESMOS Department, Sapienza University of Rome, Rome, Italy
Correspondence: [*] Correspondence to: Gianfranco Spalletta, MD, PhD, IRCCS Santa Lucia Foundation, Via Ardeatina, 306, 00179 Rome, Italy. E-mail: g.spalletta@hsantalucia.it.
Abstract: Polyunsaturated fatty acids (PUFA) of the n-3 series have been linked to brain physiology and cognitive decline, but little is known about the other components of the complex fatty acids category. Here, we compared 30 molecular species pertaining to saturated, monounsaturated, polyunsaturated, and trans fatty acids, measured in plasma by gas chromatography, in 14 patients with a diagnosis of amnestic single domain mild cognitive impairment (aMCI), 30 patients with mild Alzheimer's disease (AD), and 30 healthy controls (HC). As no participants showed neuroimaging evidence of cerebrovascular disease, patients could be considered as purely neurodegenerative. We found differences in specific components of almost all fatty acid classes except n-3-polyunsaturated fatty acids. Compared with HC, aMCI and AD patients had higher levels of arachidic (C20:0), erucic (C22:1, n-9), and vaccenic acid (C18:1, n-9) and lower levels of cerotic (C26:0) and linoleic acid (C18:2, n-6). In particular, level of linoleic acid decreased and level of mead acid increased progressively from HC to aMCI to AD patients, and they were also inversely correlated in AD and aMCI patients. In conclusion, we found a previously unrecognized linoleic acid deficiency in the early phase of neurodegeneration that was strongly supported by an increased, compensatory mead acid level. These findings suggest the importance of creating new dietary manipulation strategies to counteract disease progression.
Keywords: Alzheimer's disease, fatty acids, linoleic acid, neurodegeneration
DOI: 10.3233/JAD-122224
Journal: Journal of Alzheimer's Disease, vol. 36, no. 3, pp. 545-553, 2013
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