Affiliations: Sir James McCusker Alzheimer Disease Research Unit, School of Psychiatry and Clinical Neurosciences, The University of Western Australia; Centre of Excellence for Alzheimer's Disease Research and Care, School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Joondalup, Australia | [x] The University of British Columbia, Kinsmen Laboratory of Neurological Research, Vancouver, BC, Canada | [y] Sir James McCusker Alzheimer's Disease Research Unit, University of Western Australia, Hollywood Private Hospital, 115 Monash Avenue, Nedlands, Perth, WA 6009, Australia
Correspondence:
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Corresponding author: Nadezda Urosevic, Sir James McCusker Alzheimer Disease Research Unit, School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Australia. Tel.: +618 6304 2110, Fax: +618 6304 5851; E-mail: [email protected].
Abstract: Microorganisms, bacteria and viruses may infect and cause a range of acute and chronic diseases in humans dependent on the genetic background, age, sex, immune and health status of the host, as well as on the nature, virulence and dose of infectious agent. Late onset Alzheimer's disease (AD) is a progressive neurodegenerative illness of broad aetiology with a strong genetic component and a significant contribution of age, sex and life style factors. Both infectious diseases and AD are characterised by an increased production of an array of immune mediators, cytokines, chemokines and complement proteins by the host cells as well as by changes in the host lipid metabolism. In this review, we re-examine a dangerous liaison between several viral and bacterial infections and the most significant genetic factor for AD, APOE ε4, and the possible impact of this alliance on AD development. This connection was discussed in the broader context of lipid metabolism and in the light of different capacity of various infectious agents, their toxic lipophilic products and host lipoprotein particles for binding to cell receptor(s).
Keywords: Apolipoprotein E4, Chlamydia, Hepatitis C virus, Herpes Simplex virus 1, Human Immunodeficiency virus, LDL receptors, lipopolysaccharide, spirochetes
