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REVIEW
Year : 2019  |  Volume : 14  |  Issue : 9  |  Page : 1503-1506

Could autophagy dysregulation link neurotropic viruses to Alzheimer’s disease?


Department of Experimental Medicine, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome, Italy

Correspondence Address:
Mara Cirone
Department of Experimental Medicine, Sapienza University of Rome, Laboratory Affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Rome
Italy
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Source of Support: The work was supported by Human Herpesvirus-6 Foundation and Istituto Pasteur Italia-Fondazione Cenci Bolognetti (to MC), Conflict of Interest: None


DOI: 10.4103/1673-5374.253508

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Neurotropic herpesviruses have been associated with the onset and progression of Alzheimer’s disease, a common form of dementia that afflicts a large percentage of elderly individuals. Interestingly, among the neurotropic herpesviruses, herpes simplex virus-1, human herpesvirus-6A, and human herpesvirus-6B have been reported to infect several cell types present in the central nervous system and to dysregulate autophagy, a process required for homeostasis of cells, especially neurons. Indeed autophagosome accumulation, indicating an unbalance between autophagosome formation and autophagosome degradation, has been observed in neurons of Alzheimer’s disease patients and may play a role in the intracellular and extracellular accumulation of amyloid β and in the altered protein tau metabolism. Moreover, herpesvirus infection of central nervous system cells such as glia and microglia can increase the production of oxidant species through the alteration of mitochondrial dynamics and promote inflammation, another hallmark of Alzheimer’s disease. This evidence suggests that it is worth further investigating the role of neurotropic herpesviruses, particularly human herpesvirus-6A/B, in the etiopathogenesis of Alzheimer’s disease.


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