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Minerva Medica 2019 June;110(3):238-50

DOI: 10.23736/S0026-4806.18.05875-5

Copyright © 2018 EDIZIONI MINERVA MEDICA

lingua: Inglese

Evaluating the link between Paraoxonase-1 levels and Alzheimer’s disease development

Carlo CERVELLATI 1 , Giuseppe VALACCHI 2, 3, Veronica TISATO 4, Giovanni ZULIANI 4, Judit MARSILLACH 5

1 Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy; 2 Plants for Human Health Institute, Department of Animal Sciences, NC Research Campus, North Carolina State University, Kannapolis, NC, USA; 3 Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy; 4 Department of Morphology, Surgery and Experimental Medicine and LTTA Center, University of Ferrara, Ferrara, Italy; 5 Division of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA, USA



At present, the etiopathogenesis of Alzheimer’s disease (AD), the most common form of dementia, remains far to be fully deciphered. In the recent years, also the centrality of amyloid-β peptide in the pathogenesis of the neurodegenerative disease has been questioned and other hypotheses have been advanced. Notably, a common denominator of many of these theoretical models is represented by oxidative stress, which is widely proposed to play a role in the disease initiation and/or progression. Paraoxonase 1 (PON1) is a high-density lipoprotein (HDL)-associated enzyme that endows its carrier with multiple biological functions, including the ability to contrast oxidative damage to lipid components of lipoproteins and cells and protect from toxicity of specific organophosphorus pesticides. The peculiar multi-functionality nature of PON1 might be the key for explaining the vast epidemiological data showing a close association between low serum PON1 activity and risk of several diseases, including cardiovascular and neurodegenerative diseases, in particular AD. In this review, we discuss the possible link between PON1 with AD pathogenesis and we hypothesize eventual mechanistic pathways that could account from epidemiological observations. We also highlight the methodological issue limitation in PON1 studies that still impede to give a definitive and certain picture of its effective biological impact on human health including AD.


KEY WORDS: PON1 protein, human - Alzheimer’s disease - Oxidative stress

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