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Article type: Research Article
Authors: Odetti, Patrizioa | Piccini, Alessandrab | Giliberto, Lucab | Borghi, Robertab | Natale, Alessiaa | Monacelli, Fiammettaa | Marchese, Monicaa | Assini, Andreab | Colucci, Monicab | Cammarata, Sergioc | Tabaton, Massimob; *
Affiliations: [a] Gerontology and Geriatrics, Department of Internal Medicine University of Genova, Viale Benedetto XV 6, 16132 Genova, Italy | [b] Department of Neurosciences, Ophthalmology and Genetics, University of Genova, Via De Toni 5, 16132 Genova, Italy | [c] Department of Neurology, Galliera Hospital, Mura delle Cappuccine 14, 16128 Genova, Italy
Correspondence: [*] Corresponding author: Prof. Massimo Tabaton, Department of Neurosciences, Ophthalmology and Genetics, University of Genoa, Via De Toni, 5, 16132 Genova, Italy. Tel.: +39 010 3537064; Fax: +39 010 506938; E-mail: [email protected].
Abstract: Epidemiological and experimental data suggest that type 2 diabetes (DM2) and sporadic late-onset Alzheimer's disease (AD) share a common mechanism, that is able to produce accumulation of insulin and amyloid β42 (Aβ42), the major pathogenic events respectively of the two conditions. In 71 non diabetic patients with amnestic mild cognitive impairment we found a significant linear correlation between fasting plasma levels of insulin and Aβ42 (R=+0.25, P<0.05). The levels of both peptides were elevated in comparison to 48 age-matched cognitively normal controls. The correlation of insulin and Aβ42 plasma levels suggests a pathogenic link between DM2 and sporadic AD.
Keywords: Amyloid β42, insulin, Alzheimer's disease, type 2 diabetes, mild cognitive impairment
DOI: 10.3233/JAD-2005-8303
Journal: Journal of Alzheimer's Disease, vol. 8, no. 3, pp. 243-245, 2005
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