Role of viral infections in the pathogenesis of Alzheimer’s disease
Journal Title: Advances in Hygiene and Experimental Medicine - Year 2018, Vol 72, Issue
Abstract
Alzheimer’s disease (AD) is the most common type of dementia around the world. It primarily affects the elderly, but unfortunately neurodegenerative changes can commence at any age. Despite of the next decade of research regarding the pathogenesis of AD, its underlying causes remain unclear. Amyloid cascade theory was until recently an accepted explanation of the mechanism of AD development, according to which the Aβ42 peptide is responsible for the induction of neurodegenerative changes and inflammatory burden in the brain. As a result of recent scientific data, the amyloid cascade hypothesis became controversial. Currently, more attention is focused on the role of infectious agents and an impaired immune response during aging, that lead to the development of chronic infections and reactivation of viral latent infections. This review concerns on the recent data about the role of viruses in AD neuropathology. Numerous studies confirm an association between neurotropic viruses from the Herpesviridae family, especially human herpesvirus 1 (HHV-1), cytomegalovirus (CMV) and human herpesvirus 2 (HHV-2), and AD. The relationship between hepatitis C virus (HCV) infection and human immunodeficiency virus (HIV) and dementia is also mentioned. Viruses that enter into the brain successfully multiply in nerve cells, disturbing cellular homeostasis. Next, they activate the inflammatory response and affect the expression of numerous genes and proteins metabolism, which in turn leads to the atrophy of characteristic areas of the brain and the development of AD. Searching for the new early markers of the disease, associated with infections and impaired immune response, is a priority in developing therapies that can be implemented many years before the clinical manifestation of the disease.<br/><br/>
Authors and Affiliations
Michał Ochnik, Marta Sochocka
Keywords
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- EP ID EP396675
- DOI 10.5604/01.3001.0012.6439
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